In CD4+ T cells, CIT highlighted site-specific DNAm as a probable regulatory intermediate between risk variant-meQTLs and eQTMs at 5 risk loci (FDR < 0.05), implicating ANKRD55, JAZF1, ORMDL3, FCRL3, IL6ST, C11orf10, TAX1BP1, and GSDMB as genes with potential to confer perturbed immune function via this mechanism in RA. This evidence concerns the gene TAX1BP1 and rheumatoid arthritis.