Fine-mapping for RA and PSOR was more productive: RA had five loci mapped to credible sets with five or fewer variants, and PSOR had seven loci mapped to a single causal variant, including the TYK2 P1104A (also the T1D putative causal variant), a missense variant for TRAF3IP2-AS1 (D10N), and variants in the introns of KCNH7, DDX58, and NOS2. AS, CeD, and SLE used all available GWAS samples. This evidence concerns the gene TRAF3IP2 and rheumatoid arthritis.