However, the effects of the genetic architecture of the MHC region on PsV risk have yet to be fully elucidated. Previous studies have suggested the existence of other risk variants in addition to HLA-C∗06:02 in class I human leukocyte antigen (HLA) genes (HLA-A [MIM 142800] or HLA-B [MIM 142830]) and class II HLA genes (HLA-DRB1 [MIM 142857], HLA-DQA1 [MIM 146880], HLA-DQB1 [MIM 604305], HLA-DPA1 [MIM 142880], or HLA-DPB1 [MIM 142858]).13–18 Investigators have also studied polymorphisms of MHC class I polypeptide-related sequence A (MICA [MIM 600169]), an HLA-like gene that does not present antigen.17,19,20 However, strong and complex linkage-disequilibrium (LD) patterns in the MHC region21,22 have thus far challenged the identification of independent risk signals. Moreover, analyses focusing on the two major subsets of PsV have identified different effect sizes of associated risk alleles (including HLA-C∗06:02) between PsA and PsC, suggesting heterogeneous effects of HLA alleles on the two major subphenotypes.13–16,23