We then investigated additional HLA-variant PsV risk independent of HLA-C. When we conditioned on all classical HLA-C alleles, we observed a significant independent association at HLA-B amino acid position 67 (pomnibus = 1.8 × 10−45; Figures 2B and 3B). Stepwise regression analysis of HLA-B variants further identified an independent association at position 9 (pomnibus = 1.5 × 10−8). When we conditioned on HLA-C and HLA-B, we observed a significant independent association at HLA-A amino acid position 95 (pomnibus = 2.1 × 10−36; Figures 2C and 3C). Stepwise analysis did not identify additional association within HLA-A. When we conditioned on the effects of HLA-C, HLA-B, and HLA-A, we observed a significant independent association at HLA-DQα1 amino acid position 53 (pomnibus = 4.2 × 10−10; Figures 2D and 3D). Stepwise analysis did not identify an additional association within HLA-DQA1. When conditioning on HLA-C, HLA-B, HLA-A, and HLA-DQA1, we observed no other significant associations (p > 5.0 × 10−8; Figure 2E). These results demonstrate that PsV risk within the MHC region can be explained by combinations of multiple class I and class II HLA genes.