Based on the above-mentioned background,our study was inspired by these facts: the shared genetic architecture of RA and SLE(8–10); AFF1 and AFF3 belonging to thesame genetic family (21); the success ofreplicating the association of AFF3 with SLE by targetingpolymorphism related to RA (18); and thepotential biological function of AFF1 in lymphocyte development(11,23–25). The gene discussed is AFF3; the disease is rheumatoid arthritis.