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Generalized granuloma annulare after bacillus Calmette–Guérin vaccination, clinically resembling papular tuberculid

to the substitution of glycine 499 by serine (G499S; Fig. 1c). No mutations were found in K17, K16, K6a or K6c. No such mutation was found in her parents and the 100 unrelated controls (Fig. 1d). Three mutations have been reported in K6b, but this is the first mutation to be reported in the tail domain of PC-2. Another known similar mutation was a insertion mutation located in the tail domain of K6a in PC-1. Unlike epidermolysis bullosa simplex, the correlation between severity of disease and the location of the mutation within the keratin molecule of PC is not clear. Connors et al. detected a case of late-onset PC association with a mutation K354N in the central 2B domain of K16. Our group has reported a mutation N109D in the second half of the 1A domain of K17 with delayed onset PC-2. Terrinoni et al. reported a postzygotic mutation in the V1 domain of K16 with unilateral palmoplantar nevus and delayed onset PC-1. In this report, we found a mutation in the V2 domain of K6b associated with late onset and milder thickened nails. The patients listed above had delayed-onset PC, the milder phenotypes, and their mutation located at the less critical site of the keratins which is consistent with Connors et al. and Xiao et al.’s speculation. In conclusion, we reported a Chinese female affected with delayed-onset PC-2 caused by a novel mutation in the K6b V2 domain. The more PC patients that are reported, the more clinical data is accumulated. It will help expand the understanding of relationship between genotype and phenotype in PC and may give some clues to the cause of the phenotypic variability. ACKNOWLEDGMENTS: We thank the patient and her family for their participation in this report. The authors declare that there was no funding.