The association between Fcγ receptor type IIIa (FcγRIIIa) genotype and clinical response and/or the degree of B cell depletion in RA 9 and SLE 10 suggests that the ADCC‐type FcγR‐dependent systems (including antibody‐dependent cellular phagocytosis) are the main RTX effector mechanisms in vivo, in both RA and SLE, as previously noted for some B cell malignancies 11, 12, 13. Here, FCGR2A is linked to rheumatoid arthritis.