In this study, we fine mapped PsV risk within the MHC region. In addition to imputing variants of HLA genes, we evaluated risk of the HLA-like gene MICA by creating a MICA reference panel that empirically demonstrated high imputation accuracy. 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. To our knowledge, ours is the largest HLA fine-mapping study of PsV associations in the MHC to date and defines genetic heterogeneity between PsA and PsC subphenotypes.