is that the association signal we detected was due to the presence of regulatory rather than coding SNPs, as indeed is the case for many autoimmune diseases. 7 The data generated by the HapMap Consortium are consistent with this hypothesis, as they show that variants identified in our previous association study are in strong linkage disequilibrium with several SNPs mapping to the DSG3 promoter. The notion that alleles affecting DSG3 regulation may be pathogenic is also in agreement with results obtained in animal models, demonstrating that altered DSG3 expression can affect epidermal differentiation 8 and keratinocyte cohesion. 9 In this context, a functional and genetic characterization of DSG3 regulatory elements is now required and holds the promise to identify novel sequence variants affecting gene expression and disease susceptibility. AcknowledgmentsWe thank the PV network as well as all the patients who participated in this study.

Sarcomatoid sweat gland carcinomas are rare among cutaneous cancers, with less than 20 cases described. A 54‐year‐old woman with sarcomatoid sweat gland carcinoma of the right upper extremity suffered extensive recurrence at 15 months, unresponsive to chemotherapy. There is no standard treatment or chemotherapy regimens for metastatic sweat gland carcinoma.