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A new Robertsonian translocation, rob(l 5;25), was discovered in a Portuguese Barrosa cow. The animal (2n = 59, XX) was found by G- and R-banding to be a heterozygous carrier of a centric fusion translocation involving chromosomes 15 and 25. C-banding revealed the dicentric nature of this new centric fusion. Comparison of this new translocation with the well-known Robertsonian translocation rob(l;29), which is often found in the same breed, confirmed that two different chromosomes (25 and 29) were involved in the short arms of these two Robertsonian translocations.

the filaggrin gene (FLG) . The homozygous or compound heterozygous loss-of-function mutations p.R501X and c.2282del4 in FLG have been identified in moderate or severe IV patients from Ireland, Scotland and the USA [1] . These variants are carried by approximately 9% of European people and were also revealed to be important predisposing factors for AD [2] . Meanwhile, c.3321delA and p.S2554X mutations in FLG were identified as prevalent in Japanese IV and AD patients [3] . However, in that study the frequency of FLG mutations in the Japanese AD cohort was much lower than that seen in Europeans (5.6 and 48%, respectively) [3] . Recently, the same research group has reported additional nonsense FLG mutations (p.S2889X and p.S3296X) in Japan and extended the statistical significance of FLG null mutations in Japanese cases to 1 20% [4] . These findings imply that FLG mutations are predisposing factors for IV and AD, and show the presence of population-specific recurrent FLG mutations. In this regard, we analyzed FLG mutations in a 35-year-old Korean man who presented with a history of IV and AD since childhood. His sister and 2 daughters were affected by AD and xerosis. Marked adherent fine scales were clearly visible on his trunk. He also showed hyperlinear palms ( fig. 1 a, b). Histology revealed no keratohyalin granules in the granular layer ( fig. 2 ). We performed direct sequencing of the FLG gene in this patient, as well as screening for the previously reported mutations. Analysis revealed that he was a heterozygous carrier of the FLG mutation c.3321delA ( fig. 3 ). This mutation has already been reported by Nomura et al. [3] in Japanese cases.