We undertook functionally informed SNP-based fine-mapping analyses using the European ancestry GWAS findings, targeting all autosomal GWAS loci excluding the major histocompatibility complex (MHC) region. Twenty-four variants showed strong putative evidence of causality (posterior inclusion probability [PIP] > 0.95) at IRF4, ESR1, and FURIN (Table S2). Credible causal set sizes comprising ≤10 variants (cumulative PIP > 0.95) were identified at 224 loci, and 234/564 autosomal loci could be mapped to one or more genes (Table S2).
