The harm arises in the mating rather than in the individual, and what the hearing evidence does and does not establish
The material on this page is drawn from the Global Cat Health Survey 2026, which is where its sources and its declarations of interest are set out in full.
The papers answer where each variant sits in the gene. This part answers the question a breeder or a club arrives with: I have a cat carrying this, what do I need to know and what should I not do. It is the survey's reading of the published facts, and a reader is free to take the facts and disagree with the reading. The gene itself is on the genetics page, which explains what each variant does to it.
A cat with one copy is, on everything published, a healthy cat with a blue eye. The harm is in the mating, not in the animal. Every serious outcome in the literature, the white deaf kittens, the kittens dead at birth, the kittens never born at all, came from putting two carriers together. Not one came from a carrier bred to a non-carrier.
So the decision is never which cat to keep. It is which two cats to put together: do not mate two dominant blue eyed cats, and do not assume cats of different lines are safe together because their variants differ. The cross that produced two white deaf kittens was between two different variants.
And a carrier need not look like one. Latent carriers appear in most of these lines, so selecting against the blue eye does not select against the variant: a line can carry one for generations with nothing to breed away from, and the first sign is a mating between two cats that both looked clear. That is the strongest argument there is for testing rather than looking, and it is why this directory keeps a page of the cats a single test would settle.
| If your cat carries | What you should know | The pitfall specific to it |
|---|---|---|
| DBECEL | The best-evidenced of the six on hearing. Forty-seven cats BAER tested, no increased deafness found. In one copy this is the most reassuring row in the table | The reassurance stops at one copy. The single homozygote recorded died at birth with a cleft palate and limb abnormalities. A well-studied variant is not a safe one to double |
| DBEALT | No increased deafness reported in carriers. It is the one variant with living homozygotes: three were identified, white or almost white, and some were deaf | Being survivable is what makes it dangerous. Because homozygotes live, a programme can accumulate them without the losses that would stop it, and what it accumulates is white cats with hearing loss. It is also the variant most likely to be met in a cross, being the most widely spread |
| DBERE | This is the one with a hearing question attached. The first study confirmed unilateral and bilateral deafness by BAER in carriers. A later study tested ten more cats and found none deaf, and suggested the deafness in the original family may have come from its other genes | The two studies disagree and neither is large. Eight cats against ten. If you breed this line, BAER test and contribute the result, because the prevalence is genuinely unknown and your cats are the data that would settle it |
| DBEAGO | Breeders have reported no deafness. No cat of this line has ever had a hearing test. | Do not read the empty column as a clean one. This is the newest line and the least examined; there is no homozygote data either. Anyone breeding it is ahead of the evidence, and the honest position is that nobody knows yet |
| DBENAD | Three deaf cats were recorded among tens of dominant blue eyed kittens produced in the line, and on that basis the authors state the variant does not appear to carry an increased risk of deafness. Both halves of that belong together: deafness has occurred in this line, and the finding is that it occurs no more often than it would anyway. It is the breeder's own record and not audiometry, so no cat here has been BAER tested. Thirty-nine carriers genotyped and every one heterozygous | The pitfall here is invisible and it is the worst on this page. The homozygote dies in the womb. You will never see a dead kitten, an abnormality or anything to investigate. You will see a slightly small litter, which nobody writes down against a gene. A programme can mate carrier to carrier for years and the only trace will be a quarter of every litter that was never born |
| DBEMARU | No hearing data of any kind exists for this line. The paper states it in those words | The one homozygote recorded was abnormal and died at birth. With no hearing data and one mating's worth of homozygote data, every statement about this variant is provisional |
| DBEcDc, DBExHW | Identified in China and a commercial laboratory sells a test for each. No paper has been published on either | A test exists but the evidence behind it is not public, so nothing about hearing, homozygotes or health can be stated here at all |
| The Igor line | The determinant is at PAX3 on the evidence, but no allele has been published and no test is on sale. Four named variants have been excluded from the line by assay | There is nothing a breeder can buy. A cat of this line cannot be cleared or confirmed, which makes pedigree the only tool available and makes an accurate pedigree worth more here than anywhere else in the survey |
This is the question a breeder or a club actually needs answered, and the papers do support an answer. It has two halves, and they point in opposite directions.
In a single copy, the published evidence is more reassuring for the two non-coding variants. A cat with one copy of DBECEL or DBEALT has a normal protein and simply less of it. The authors state that deafness has not been associated with either variant in heterozygous cats. Of 47 tested Céleste cats, three were unilaterally deaf and none bilaterally, and all three had a history of ear disease that would explain it.
The coding variants truncate the protein, and one of them does carry a hearing association. DBERE was reported with unilateral and bilateral deafness confirmed by BAER in heterozygous Maine Coons. The 2025 follow-up then tested ten more cats of that line and found none deaf at all, and concluded that deafness is associated with the variant but that further data are needed to know how often, raising the possibility that the deafness in the original pedigree came from modifying genes in that family rather than from the variant itself. That is where the evidence currently stands and it is not a closed question.
And the difference disappears entirely as soon as a cat has two. This is the part that matters most for a mating decision. In one copy the six behave differently; in two copies not one of them is safe, and the non-coding pair is not the gentler option:
So the honest answer is: in one copy, yes, the non-coding pair carries less recorded risk; in two copies, no, and the question stops being about which variant and starts being about not doubling any of them.
No deafness reported is not the same as no deafness. Two of the six have no hearing evidence at all. For DBEAGO, breeders reported no deafness but no BAER testing was done. For DBEMARU, the paper states plainly that no data is available on the hearing status of any cat in that line.
A variant with no hearing data is not a safe variant. It is an untested one, and a club writing a rule on the strength of an empty column would be writing it on nothing. The clean way to use this page is to read across a row and notice which cells are empty, because those are the cells that tell a breeder what is not yet known about the cat in front of them.
These two things are easily mistaken for one another, and a single score cannot carry both. How much is known about a variant and how risky that variant is are different questions. A variant that forty-seven cats have been tested for is well described; a variant nobody has tested is not thereby safe, and not thereby dangerous. It is unmeasured.
So this table splits them. The left column is what was observed. The right column is the size and the kind of the evidence it was observed on. Read them together or not at all.
| Variant | In one copy, what was observed | How hard anyone looked | In two copies, what was observed | How hard anyone looked |
|---|---|---|---|---|
| DBECEL | No increased deafness. Three unilaterally deaf, none bilaterally, and all three had a history of ear disease | 47 cats, BAER tested. The largest hearing dataset on any of these variants | One kitten. Died at birth of a cleft palate, with limb abnormalities | One mating. One kitten is one kitten |
| DBEALT | No increased deafness reported | No BAER count is published for heterozygotes. The authors describe the data as limited | Viable. White or almost white, and some of them deaf | Three homozygous cats identified. The only variant here with living homozygotes to look at |
| DBERE | Deafness confirmed by BAER, unilateral and bilateral, in the original report. A later study found none in ten further cats and suggested the family's other genes may be responsible | 8 cats in the first study, 10 in the second, and they disagree. The authors state further data are needed to know the prevalence | None has ever been recorded | No mating has produced one, which the authors read as lethal. That is an inference from an absence |
| DBEAGO | No deafness reported by the breeders | NOBODY HAS TESTED ANY OF THEM. The paper states plainly that no BAER testing was performed. This cell is empty, not reassuring | Not known | All thirteen carriers were heterozygous. The line is too recent for the question to have arisen |
| DBENAD | No increased deafness on the breeder's data. Three deaf cats among tens of kittens | 39 cats genotyped, but the hearing figure is the breeder's record and not BAER. A different kind of evidence from the CEL row, in the same column | Lost before birth. The litter proportions show it | 39 cats and not one homozygote. A strong absence, and still an absence |
| DBEMARU | Nothing is known | NO HEARING DATA EXISTS FOR THIS LINE AT ALL. The paper says so in those words | One kitten, abnormal, died at birth | One mating. As with CEL, one kitten |
Read down the third column and the point makes itself. Forty-seven cats were put through a hearing test for one variant. For two others, not one cat has ever been tested. Those are not six comparable rows.
And read the fourth column with the same care. Three of the six have a homozygous outcome resting on a single kitten. One rests on an absence. Only DBEALT has living homozygotes anyone has been able to examine. A table that prints lethal beside viable in the same typeface is not wrong, but it is giving one kitten and three cats the same weight.
The rule the survey applies, and would ask a club to apply. Where a cell is empty, write that it is empty. Do not colour it green and do not colour it red. An untested variant is not a safe one and it is not a dangerous one; it is untested, and the only thing that changes that is testing.
These variants are dominant, so one copy shows. The question that matters for breeding is what two copies do, and the answer is not the same for every variant. This is what the papers record.
| Variant | Two copies | What was observed |
|---|---|---|
| DBEALT | Viable | Three homozygous cats identified, all white or almost white. No abnormality except that some were deaf |
| DBECEL | Died at birth | One homozygous kitten, white, died of a cleft palate just after birth, with limb abnormalities |
| DBERE | None ever recorded | No homozygote has been reported, which the authors read as the homozygous state being lethal |
| DBENAD | Lost before birth | No homozygote among any cat tested. The proportions in the litters indicate they are lost in the womb, and repeated matings between two carriers never produced an abnormal kitten because the affected quarter is never born |
| DBEMARU | Died at birth | One abnormal kitten from a carrier by carrier mating, confirmed homozygous |
| DBEAGO | Not known | All thirteen carriers tested were heterozygous. The line is too recent for the question to have arisen |
And one copy each of two different variants is its own case. A mating between the Céleste and the Altai produced two white, deaf kittens carrying one copy of DBECEL and one of DBEALT. They lived. The authors state that cats carrying those two alleles are viable but at high risk of deafness. A DBECEL by DBERE kitten, by contrast, died at birth with an enlarged head and contracted limbs. Two dominant blue eyed cats of different lines are not a safe mating on the ground that the variants are different.
Everything above is what the papers establish. This section is the survey's reading of what follows from it, and it is marked as a reading rather than a finding so that a reader can disagree with it while still using the facts.
One. The trait is not one thing, and a rule written about blue eyes is a rule written about eight different things at once. Registry requirements that trigger on the colour of an eye cannot distinguish a non-coding insertion with no recorded deafness from a nonsense variant that truncates the protein, or from a deletion of the whole gene. They are not the same risk and they should not carry the same rule. A requirement that names the variant, and not the eye, is the first thing the survey would ask a registry to write.
Two. A test result is only as wide as the panel it was run on. An assay for DBEALT says nothing about DBECEL, even though the two lie 1 747 bases apart in the same intron. A panel run in 2024 could not have covered DBEAGO, DBENAD or DBEMARU, because they were not yet described. A cat is not clear of dominant blue eyes; it is clear of the variants that were on the panel on the day it was tested, and this register grades several results that have been read more widely than that.
Three. The mating is where the harm lives, not the individual. A cat with one copy of any of these is, on the published evidence, a healthy cat with a blue eye. Put two of them together and the published outcomes are white kittens, deaf kittens, kittens dead at birth, and kittens never born at all. That is true whether the two copies are of one variant or of two different ones. It is the single most actionable thing on this page: the decision that matters is not which cat to keep, it is which two cats to put together.
Four. Some of the harm is invisible by construction. Where the homozygote dies in the womb, as with DBENAD, the breeder sees no dead kittens and no abnormality. They see a slightly small litter. A programme can double a lethal allele for years and the only sign will be litter size, which nobody records against a gene. This is the argument for recording the variant on the pedigree rather than trusting that a problem would have been noticed.
Five. A carrier need not show the trait. Latent cats appear in most of these lines: they carry the variant and their eyes never turn blue. Selecting against the blue eye therefore does not select against the variant, and a line can be carrying one for generations with nothing visible to breed away from. Only a test finds these cats, which is why this register keeps a latent-lines page at all.
Six. An empty cell is not a safe cell. Two of the six variants have no hearing data of any kind. A club that treats absence of reported deafness as evidence of no deafness will write a rule on nothing, and will have to unwrite it when the data arrives. The honest position for an untested variant is that it is untested.
Seven, and this is the one that will age. Six variants were characterised between 2024 and 2026, and two more are identified but unpublished. The gap between a founder appearing and its allele being named has run from twenty-nine years down to seven, and it has not closed. Cats bred during that gap were bred blind, and their descendants inherit that. A registry framework that can only act once an allele is published is a framework that acts a decade late every time, and the remedy is a registration class that records a line as untested rather than as clear.
A cat with one copy of one variant is, on present evidence, unaffected. What is recorded below is what happens when a kitten inherits two. The two rows of the table are the two ways that can occur.
| Genotype | What is recorded | Evidence |
|---|---|---|
| Two copies of the same variant, the homozygous state | ||
| DBECEL (Roxi) × DBECEL (Roxi) | Lethal at birth | One homozygote is on record, genotyped, and it died at birth of a cleft palate. A white kitten of the Céleste programme, homozygous for the insertion. A cleft palate is a failure of the facial bones to close, and PAX3 governs the same embryonic cell population that builds them, so the defect and the eye have one origin. LOOF prohibits Céleste to Céleste mating on this basis. Abitbol, Couronné et al., Animal Genetics 2024;55:670-675 |
| DBERE × DBERE | Embryonic lethal | Reported. No homozygote was observed in either published BAER series; both genotyped their animals and found none |
| DBEALT × DBEALT | Survives, but white or nearly white and reported at risk of deafness | Observed in the founding Altai programme, where homozygotes were “most often deaf”. Three homozygotes are described in the literature |
| DBEAGO × DBEAGO | No data | Published June 2025. No homozygote reported |
| DBEcDc, DBExHW | No data | Identified 2025, unpublished |
| DBENAD × DBENAD | Lethal in utero | No homozygote has been found alive. 39 blue eyed cats of the line and 47 controls were genotyped and not one was homozygous. Repeated matings between two blue eyed cats produced no abnormal kitten; it is the proportion of blue eyed to non blue eyed kittens in those litters that shows the loss, so a breeder sees a small litter and nothing else. No test is on sale for it |
| DBEMARU × DBEMARU | Lethal at birth | One homozygote is on record, genotyped T/T, and it did not live. An abnormal kitten out of two blue eyed parents, dead at birth. All 14 blue eyed cats of the line are heterozygous. This is the only dominant blue eye variant for which a homozygous animal has been genotyped and recorded as lost, rather than inferred from litter proportions. No test is on sale for it |
| Malvina line | Lethal | Reported. No causal variant identified, so no test can predict it. Seven blue eyed cats of the line have been genotyped and are wild-type for both DBENAD and DBEMARU |
| Igor line, PAX3, allele not published | No data, and it is a different kind of no data from the rows above | No homozygote has been reported, and none could be confirmed if one were born. Every other line in this table can be read either way: a homozygote is genotyped, or its absence from a genotyped cohort is itself the finding. No test for this determinant is on sale, so a kitten carrying two copies could not be identified by any laboratory now selling a panel, and a breeder losing such a kitten would have nothing to record beyond the loss. This is one of the largest lines in the register, so matings between two of its blue-eyed cats are likely to have occurred; what is absent is not the mating but the means of reading it. The compound row below is the only cross involving this line that has been recorded at all |
| Pillowtalk-Foreigner and Gosha lines | No data | No data on homozygosity and none on deafness for either line. The search for the variant is reported ongoing for Pillowtalk-Foreigner, by a German research team, and to have just started for Gosha. Neither line has a causal variant identified, so no test can predict either state. Abitbol M, CORIN and DBE variants in cats: what we know and what remains to be explored, World Cat Federation, 2026. A presentation and not a published paper. That presentation covers the CORIN gene alongside the DBE variants; CORIN is outside the scope of the survey and is not examined here |
| One copy each of two different variants, the compound heterozygous state | ||
| DBECEL (Roxi) and DBEALT | Two kittens born deaf | Both genotyped |
| DBECEL (Roxi) and DBERE | One kitten died at birth, with limb contractures and an abnormal head | Presumed genotype, not confirmed |
| DBEALT (Seymour) and the Igor line, PAX3, allele not published | Two daughters born white, blue eyed and deaf | A first-hand account from the breeder who made the cross, supplied 30 August 2026, and not confirmed by a genotype. She held both lines and made the cross deliberately. In her own words: “This is a daughter that resulted from two lines. There were two of them, both deaf. I gave the second one to a friend, and she still works with her offspring. I bred Josephine and sold the offspring as pets. The line doesn’t continue any further.” She states separately that she has stopped breeding the Igor line. This is a breeder statement and not a clinical record: there is no audiometry, no veterinary report and no date for the hearing finding, and the survey enters it as reported for that reason. Both daughters showed the phenotype the published compound heterozygotes showed: white and deaf. Neither parent is white and neither is deaf. The elder is coded 02 on her certificate, which is the nearest white-spotting figure a registrar has for a white kitten, but she carries no colour patch anywhere. No test for the Igor line is on sale, so this pairing cannot be predicted by any panel now sold |
The last row repeats the configuration of the published case, which is what makes it worth recording rather than filing as an anecdote. In Abitbol et al. 2024 the dam was latent: she carried DBEALT, showed no blue iris, and the mating produced two white deaf kittens. In the 2026 report the dam is again a cat showing no blue eye, recorded latent by the compiler, standing six generations below Nikita'l Seymour by unbroken parent links, bred to a blue-eyed sire of a second line. Two daughters, both reported deaf. A single copy of DBEALT does not do this: nine genotyped heterozygous carriers of it were BAER tested at Glasgow and all nine heard normally in both ears. The reported harm in the survey is confined to animals standing below two determinants.
And that carries an inference about the Igor determinant. A compound heterozygote is two different alleles at one locus, and the published case is the PAX3 compound: the two white deaf kittens carried DBECEL and DBEALT, both PAX3 variants, one on each chromosome. A cross to a second line producing the same outcome is evidence that the second determinant is also at PAX3, because a variant at another locus would give a double heterozygote at two loci and not a compound at one. Every determinant with a published variant is a PAX3 variant, six of six, so the prior is already high and this cross is consistent with it. The step that settles it is a PAX3 screen on one Igor-line cat, a targeted read of a single gene rather than the whole-genome discovery project the survey has been asking for, and one a commercial variant panel does not perform: a panel reports the variants already named and returns clear on a ninth. The white these animals carry remains on the record as an alternative the pedigree cannot exclude, and the PAX3 read is what distinguishes them.
Where else can this happen. Four pairs of variants already have animals standing in both lines of descent: DBEALT with DBECEL, 84 animals across ten catteries; DBEALT with DBERE and DBECEL with DBERE, five animals each; and DBEALT with the Igor line, the two sisters above. Not one animal in any of the four has been tested for the second variant it could be carrying. The traces, the catteries and the counting rule are on the variant trace page, and the Igor case is worked through in the Igor case study.
Reading the table has two consequences for a breeder. Every row in the lower section involves two different variants, which is the combination a breeder working carefully within a single line will not produce, and which arises when cats from two separate lines are brought together. And the empty cells matter as much as the filled ones: for four of the eight variants nobody has recorded what two copies does, so a mating that would produce one cannot be assessed at all.
The mating to be avoided is therefore variant to variant, whether the two variants are the same one twice or two different ones. As the lines mix across breeds, that mating becomes easier to make unintentionally.
The clearest illustration of that principle is a breed that no longer exists. The Topaz was founded deliberately on two different dominant blue eye variants. Its two founding studs came from the same Kazakh breeding programme: Roxi Darlin, carrying DBECEL (Roxi), and Nikita'l Seymour, carrying DBEALT. The published description records that the breed was created using both, thereby combining two DBE lineages. The Topaz has since been discontinued. The full history of those two cats, and of the breeds created from them, is the subject of case study two of the survey.
A breed founded on two variants will produce compound heterozygotes in successive generations by design rather than by accident. A compound heterozygote is a cat with one copy each of two different variants, and it is the state in which harm is documented. Two kittens genotyped as compound heterozygous for DBECEL and DBEALT were white and deaf. A further kitten presumed to carry DBECEL and DBERE died at birth with limb contractures and an abnormal head.
The compound heterozygote is evidenced, not inferred. Abitbol et al., Animals 2024;14:1845 reports a five-kitten litter born to two DBE parents with DNA held for both parents and four kittens: a latent dam of the Seymour line heterozygous for DBEALT, a sire heterozygous for DBECEL, one kitten heterozygous for each allele, and “the two white and deaf kittens were compound heterozygous for both DBECEL and DBEALT alleles”. The paper's own conclusion is that such cats “are viable but are at high risk of deafness” and that “breeders are warned that mating two DBE cats from the Roxi and Seymour origins may be deleterious”.
The dam was latent. She carried DBEALT and did not show the blue iris, so a rule triggered by eye colour would not have reached her, and the mating that produced two deaf kittens would have been permitted. And the DBEALT variant was itself identified from the whole-genome sequence of one of those two deaf kittens.
In later generations of the Topaz, kittens were born whose irides were so dark they read as black, and on close inspection were a very dark olive green. Six were born, from particular parent combinations. All six died of infections that were successfully treated in their normal littermates. The account concludes that they carried a defect of the immune system alongside the eye colour, and records that the lines producing the trait were sterilised.
The homozygote explanation was considered and set aside on stated grounds. None of the six carried the white distribution characteristic of homozygotes, none was deaf, and no other indication of homozygosity was present. The cause given is a mix of the two genes, DBEALT and DBECEL.
This is the strongest reported instance of compound heterozygote harm in the survey, and it is stronger than the deaf kittens on three counts. It carries a visible marker, the black iris, so the state can be recognised without a test. It carries a distinct clinical outcome, failure to survive infections that littermates survived, which is not deafness and not neonatal death. And the competing explanation was examined and excluded with reasons given rather than left unaddressed.
What it is not. It is a breeder account and not a laboratory result. None of the six was genotyped, the lines are sterilised, and the breeding records were lost with the computer that held them. Six animals is a small number and infection has many causes.
Two things nonetheless follow that do not depend on accepting the cause. The observation was made before any of the variants had been named, so it cannot have been shaped by the literature. And the same account asks the question the survey asks, in its own words, of the high-white cats: which of the two genes are they homozygous for, “could they be homozygous for both genes?” A breeder working without a test had reached the compound heterozygote question from the phenotypes alone.
Source: messybeast.com, Blue-Eyed Breeds: Topaz (Ukraine), the Seymour DBEALT and Roxi DBECEL genes, 2016 to 2026, supplied to the survey on 15 August 2026. A breeder account throughout; no genotype appears in it.
No published source states why the Topaz was discontinued. What can be stated is that the mechanism was present in the breed's foundation and that the documented harm arises in precisely that pairing.
If the association holds, the Topaz has evidential value disproportionate to its size, because it represents a cross that could not ethically be designed. It indicates that the risk in these variants lies not in carrying one but in holding two within the same population. The rule that follows is neither a ban on blue-eyed cats nor a ban on carriers, but a ban on combining two variants, whether the same variant twice or two different ones.
That rule cannot be enforced with a single-variant test. To know whether a proposed mating puts two variants together, a breeder has to know which variants both cats carry, and a test that looks for one variant reports only on that one. A cat clear for DBERE may still carry DBEALT: the mating that produced the two deaf kittens would have passed a DBERE test on both parents. The seven products on sale cover between one and five variants each, so they are not interchangeable, and a rule that does not say which variants must be covered has not specified the test it is asking for.
One of the seven products is sold under the name Deafness in cats with DBE. It is a DNA test. It reports whether the cat carries the DBERE variant. It does not report whether the cat can hear, and no DNA test can, because hearing is measured by a BAER recording at a veterinary practice and not by a cheek swab in the post.
The name assumes the very link the test is being sold on, and that link has since been qualified in the peer-reviewed literature. It rests on a series of eight affected cats reported when the variant was first described, in Rudd Garcés et al., G3 2024. A later study, Abitbol et al., Animal Genetics 2025, tested ten more cats carrying the same variant, from different lines, and found that all ten heard normally in both ears. The product name reflects the first paper and not the second.
A registry writing a requirement has to say which of the two it wants, because “a DBE test” and “a hearing test” are different things with different costs, different providers and different answers. A rule that asks for the wrong one will be satisfied by a result that does not address the risk it was written for.
Two breeders may each advertise a blue-eyed British Shorthair, using the same breed name and describing the same eye colour, while one cat carries DBECEL (Roxi) and the other DBEALT. Nothing a buyer can see, and nothing on either advertisement or either pedigree, distinguishes the two.
This happens because breeding cats move between catteries. A variant enters a breed through a single outcross and kittens from that line go to other breeders; a second variant enters the same breed later through a different outcross made by a different breeder. Within a few generations the breed holds both variants, in different catteries and often in different countries, described in identical terms. The same confusion now occurs one level down. A single named line may contain more than one variant, and the breeder-created names built on the trait, among them Azul, British Ice, Heavenly Eyes, Pantherina and Pharaoh, are names for an appearance rather than for a variant, so two cats sold under one of those names need not carry the same thing either.
The first consequence is evidential, and it governs how the breed table in the survey should be read. PAX3 DBE by breed, on the Laboratories page, records the variants that have been found somewhere in each breed. It does not state that the breed is uniform. The British Shorthair row carrying DBEALT does not mean that blue-eyed British Shorthairs are DBEALT cats; it means at least one was. This also explains how competing breed lists may both be accurate: if DBECEL (Roxi) and DBEALT are both present in the British Shorthair in different catteries, a list naming either is correct and a list naming only one is incomplete.
How these variants are governed turns on the distinction below.
The only instrument that closes that gap is a genotype recorded against the individual animal and transferred with it when it is sold, which is why that requirement appears twice in the protocol below.
Such a requirement fails in both directions, and both failures are documented rather than hypothetical.
It misses carriers. A latent cat carries a variant and never displays a blue eye, in some cases with no white marking either. Latent cats are recorded by genotype in Abitbol et al., Animals 2024;14:1845, Table 2, two in the Seymour lineage, three in the Nanotigr and one in the Roxi, and in Abitbol, Couronné et al., Animal Genetics 2024;55:670-675, Table 1, one Céleste. One latent queen was the dam of the two deaf compound heterozygotes. Under a requirement triggered by eye colour she would have bred without restriction.
It restricts cats that carry nothing. Blue eyes arise independently through the white spotting allele and through the colourpoint allele. The working rule used by many breeders, that a blue eye in a coloured coat indicates DBE while a blue eye in a white cat indicates white spotting, is incorrect: a documented mating between two cats carrying no DBE variant, one of them carrying white spotting, produced a blue-eyed offspring with parentage confirmed by DNA.
A ban on blue or odd eyes therefore excludes cats that present no risk while leaving the carriers that do. It regulates the appearance of the problem rather than the problem.
It also removes the evidence that would settle the question. Registration is the only independent certification of parentage a pedigree cat has, and a claim about descent that rests on a breeder's own record does not meet the standard applied at the higher tiers of peer review. Closing registration to a trait therefore ends the certified record of the line at that generation, while the cats themselves continue to be bred. The mechanism, its two consequences and the registration class that would resolve it are set out in the survey under the heading what a registry certifies, and what a ban removes.
The deafness evidence is set out in full below because the misstatement of it is now more widely circulated than the finding itself, including by a commercial testing company and by the general purpose chatbots most breeders will consult first.
The claim. That DBERE carries a very high risk of deafness or hearing loss even in single-copy heterozygous carriers.
Its source. Rudd Garcés et al., G3 2024, 10.1093/g3journal/jkae131, the paper that first described the variant. It carried out BAER testing, the recording that establishes whether an ear responds to sound, on ten Maine Coon cats of the Rociri Elvis line. All eight of the blue-eyed cats returned abnormal waveforms: three were deaf in one ear and five were deaf in both. Read on its own, that is eight affected out of eight.
The later study, which qualifies it and is far less often cited. Abitbol et al., Animal Genetics 2025, 10.1111/age.70020, published 3 June 2025, BAER tested a further ten Maine Coons carrying the same variant. They are not the same cats and not the same branch. The variant is restricted to the lineage founded by Rociri's Elvis, so both cohorts descend from that founder. The 2025 cats come from two branches of it, under the BigBoots and Joyfield prefixes, across three generations. Six carried the variant and four did not, and all ten heard normally in both ears.
How the two results can be reconciled. If the variant itself caused the deafness, the second group would have been deaf as well. The authors attribute the deafness in the 2024 group to modifying alleles elsewhere in that family's genetic background rather than to the variant itself: to something those cats inherited that was not linked to the PAX3 gene. A modifying allele is a variant at some other gene which alters how a first variant is expressed. On that reading the eight deaf cats were deaf because of what else that one family happened to carry, and not because of DBERE, which would explain why a second group carrying the same variant, from a different branch of the line and without that background, heard normally. The authors state that further data are required before a prevalence can be given.
A second explanation is available and is raised by the survey rather than by the authors: the affected cats may have carried a second DBE variant that had not been identified when the 2024 paper was written. DBEAGO was not published until June 2025 and two further variants were identified later that year, so a compound heterozygote could not have been recognised as one at the time. A compound heterozygote, carrying one copy each of two different variants, is the state in which deafness is documented above, which makes the possibility worth testing rather than assuming. Either explanation would account for the discrepancy, and neither has been established.
A mechanistic objection to the causal claim, from the geneticist who described most of these variants. “PAX3 is involved in embryonic development. In newborns and adults, it plays only very minor roles: it helps maintain populations of muscle and pigment stem cells. Nothing has ever been demonstrated regarding its role in immunity or in diseases unrelated to the development of muscle, nerve and pigment cells.” On that basis it is considered unlikely that the health problems and deaths reported in these lines are attributable to PAX3. An alternative explanation is a genealogy effect: that cats from these bloodlines carry a genetic background predisposing them to those problems, and that this background is inherited independently of the PAX3 variant they also carry.
The defensible position. Pooling both studies gives eight deaf among fourteen BAER-tested carriers, all from one line. Deafness is associated with DBERE and its prevalence is undetermined. It is not established that a heterozygous carrier is at very high risk.
The claim as usually stated goes further than that, and the extra distance is worth pointing out. It says the risk is high even in cats with a single copy. Putting it that way tells the reader that the single copy is the mild case and that two copies would be worse. Nothing supports that comparison, because no homozygous DBERE cat has ever been observed. Both studies genotyped their animals and neither found one, which is consistent with the report that two copies are lethal before birth. A claim about a genotype nobody has seen is not a finding.
Why the overstatement matters. An overstated harm is not a safe error, and the reason is specific to this trait. A breeder can see whether a cat hears. What a breeder cannot see is whether it carries the variant, which is the only thing the DNA test reports.
So a claim that carriers are probably deaf is contradicted by the hearing carriers already in the cattery, and two responses follow, both unhelpful. Some breeders conclude that the DNA test is not worth buying, since it appears to predict something they can already see is untrue. Others take the claim at face value and withdraw from breeding cats whose hearing is demonstrably normal, on the strength of a genotype.
There is a further cost. One finding here is sound: combining two different DBE lines produced deaf and dead kittens. That finding bears directly on how these cats are bred. When breeders discover that the deafness claim was overstated, they have reason to doubt the rest, and the sound finding is discarded with the bad one.
Deafness is the reason dominant blue eyes is treated as a welfare question rather than as a colour. Hearing is established by a BAER test, a brainstem auditory evoked response recording, which measures the response of the hearing nerve to a stimulus in each ear separately. It yields a result in a kitten or in an animal that will not co-operate with other forms of hearing assessment, and it is the only method that detects unilateral deafness.
For DBEALT no such testing had been carried out. The published papers list the DBEALT lines with hearing recorded as assumed normal, and state the reason: no BAER recording existed for any of those animals. The literature therefore carried an assumption in place of a measurement, for the variant most widely distributed in the British Shorthair.
Fourteen British Shorthair and British Longhair cats of a DBEALT line, nine carriers and five wild type relatives, were BAER tested at the Neurology and Neurosurgery service of the Small Animal Hospital at the University of Glasgow on 17 and 24 September 2024, on a TruTrace EMG system, each ear recorded separately at 80 and 100 dB. All fourteen heard normally in both ears. The carriers spanned silver and golden backgrounds and ages from two months to three years, and one of the nine was a latent cat whose carrier status was established only by DNA testing. To the author's knowledge this is the first BAER series in DBEALT British cats.
All fourteen animals were genotyped, the nine carriers heterozygous and the five relatives wild type, so the result applies to the heterozygous state only, which is the state in which the breed is ordinarily maintained. No homozygote occurred in the cohort, and only three DBEALT homozygotes have been described, two Altai and one Nanotigr, all white, with deafness in some of them, in Abitbol et al., Animals 2024;14:1845, Table 2. The cohort is small and drawn from a single breeding programme, so the result is preliminary.
The prevention control at the end of this page rests on one proposition: that a cat can carry a PAX3 variant, show no blue eye at all, and pass the variant on. Every registry rule the survey coded triggers on the colour of the eye, so none of them can see such an animal. The proposition is established by genotype in Abitbol et al., Animals 2024;14:1845, Table 2 and Abitbol, Couronné et al., Animal Genetics 2024;55:670-675, Table 1. A mating in a British Shorthair programme demonstrates it directly.
The published position first. Latent carriers are a genotyped fact and not an inference. In the DBEALT lines, three Nanotigr cats and two of the Seymour lineage were found heterozygous for the insertion while showing no blue eye. One Celestial cat is likewise heterozygous for DBECEL (Roxi) without the phenotype, and in 2025 two latent cats were identified in the DBERE Maine Coon line, where none had been reported before. The 2026 paper then records latent cats in the DBENAD and DBEMARU lines as well, describing each phenotype as heterochromia or two blue eyes, minimal to no white spotting, and the presence of latent cats. Latency is therefore published in five of the eight variants, each of which arose separately: DBECEL, DBEALT, DBERE, DBENAD and DBEMARU. It is a property of the trait and not a peculiarity of one line. The same round of genotyping found no latent cat in the Agostino line, which is a result and not a gap: cats of both Maine Coon lines were tested for both variants, and the latents fell on one side. The two Chinese variants have no phenotypic description published at all.
The mating. A latent British Shorthair queen, a black smoke carrying no blue eye, was bred in May 2024 to a carrier male of the same line. Of four kittens, two carry the trait and two do not. A cat that no eye-colour rule could have identified produced blue-eyed offspring.
The design matters: it is the control operating voluntarily. On present evidence the harm arises when two variants meet in one animal, so a carrier-to-carrier mating is the pairing the proposed control exists to prevent. Pairing a latent carrier with a carrier answers the transmission question without making that pairing. The queen's own certified pedigree carries no eye code, and neither does the sire's, though his sire is coded 61 and his great-granddam 69: a registry reading either document would see nothing at all.
Two limits apply. This is one litter of four in one programme, so it demonstrates that transmission from a latent carrier occurs and establishes no rate. And the queen's carrier status was known only because she had been DNA tested; had she not been, the litter would have appeared as blue-eyed kittens from an ordinary-eyed mother, which is how such litters are ordinarily recorded and why the register holds so many untested possible carriers.
The animals in this series were genotyped for the Inhibitor locus, which produces the silver coat, as well as for PAX3. Coat state is therefore recorded against each cat by genotype rather than by description, and the same practice was applied to every cohort assembled under this prefix, including the blood pressure trial reported below.
Silver is the coat in which a blue eye is selected against and has been written down as green, and in which white spotting is hard to see, so a cohort described as silver by eye inherits both problems and a cohort genotyped at the Inhibitor locus does not. Silver is also the single most frequent coat among the founding and first blue-eyed cats in the survey's register, at 11 of 29, the background against which most of the identified variants are observed.
Blood pressure was measured in the same population. Forty-three British Shorthair and British Longhair cats spanning three generations of the line carrying DBEALT were entered into a blood pressure trial, forty-one of them analysed, with the animals genotyped for PAX3, for the CORIN copper variant and for the Inhibitor locus. Readings were taken by an independent veterinary practice on unmedicated and unanaesthetised cats and signed off by an Official Veterinarian. No statistical relationship was found between blood pressure and CORIN copper genotype, and no blood pressure abnormality was identified in the DBEALT carriers. The trial is set out in full in registries and research.
The coat of every founding cat, and why a blue eye in a silver coat is recorded as green and its white spotting not seen at all, are set out under silver coats on the latent lines page.
Test every line, and test by genotype rather than by eye colour.
One of the nine carriers in this series was a latent cat: it carried DBEALT, showed no blue eye, and its carrier status was established only by DNA testing.
The DBEALT series is cited as a released summary statement: Abitbol M, Cloquell A, Kaczmarska A, Holmes K, Macaulay K. BAER hearing screening in British Shorthair and British Longhair cats carrying DBEALT: Summary Statement. Belle Ayr Cats, 3 June 2025. It is not peer reviewed. Its method and its cohort, cat by cat, are reproduced in the sources. The ten Maine Coon results from the same testing sessions are published: they are the BAER data reported as Table 2 of Abitbol et al. 2025, on which the author is a named co-author.
The mechanistic passage above is the assessment of Prof Marie Abitbol, VetAgro Sup, who described six of the eight variants. The three sentences in quotation marks are her wording; what follows them, including the genealogy effect, is a summary of her position and not a quotation. Rudd Garcés et al., G3 2024, 10.1093/g3journal/jkae131, Results, clinical investigations. Abitbol et al., Animal Genetics 2025, 10.1111/age.70020, Table 2 and pages 3 to 4. The 2025 BAER cohort is the author's own; see the declaration of interest in the accompanying paper.
This is one of 6 recommendations about where to spend a test. The other five are test the cats whose status cannot be seen, on Findings, trace the descendants of the unmapped lines, on Spread across breeds, screen PAX3 in one cat of an unmapped line, on Findings, test the white cats, on Latent lines and test one cat in each cattery holding two variants in one breed group, on Variant trace. A further three recommendations, about how a registry writes the trait down, are on Recommendations.
Registries have attempted prevention control, and the intention is correct. What is absent is a protocol matched to the behaviour of the variants.
Sources for this section: Abitbol M. CORIN and DBE variants in cats: what we know and what remains to be explored. Presentation to the World Cat Federation, 2026, VetAgro Sup, Campus vétérinaire de Lyon. Abitbol et al., Animal Genetics 2024, 10.1111/age.13433. Rudd Garcés et al., G3 2024, 10.1093/g3journal/jkae131. Abitbol et al., Animals 2024, 10.3390/ani14131845. Abitbol et al., Animal Genetics 2025, 10.1111/age.70020. Declaration of interest: the author of this directory is a co-author of the 2025 paper cited above.