Our study identified multiple HLA-C∗06:02-independent risk variants of both class I and class II HLA genes for PsV susceptibility (HLA-B, HLA-A, and HLA-DQA1), but no apparent risk attributable to MICA. We also observed that risk heterogeneity between PsA and PsC could be explained by polymorphisms of a single amino acid site encoded by HLA-B, suggesting that different genetic architectures underlie the overall risk of PsV and that of its subphenotypes. This evidence concerns the gene MICA and pancreatic serous cystadenoma.