Here, we were able to successfully decompose the genetic architecture of PsA and PsC to a shared component and a subphenotype-specific component. Our study demonstrates that the HLA gene associated with the risk heterogeneity between PsA and PsC (HLA-B) is distinct from the HLA gene most associated with overall PsV risk (HLA-C). Previous studies have reported that HLA-C∗06:02 has different effect sizes for PsA and PsC, naturally leading to a hypothesis that the heterogeneity is driven by the difference in HLA-C, the major risk factor.13–16,23 However, our observation is more concordant with a model where the two PsV subtypes generally share the same risk alleles, including HLA-C∗06:02, but differ at a specific locus that contributes to subtype differences.