However, when activated undesirably, the same mechanism of FcγR-mediated cytokine induction is responsible for excessive inflammation as observed in autoimmune diseases that are associated with IgG autoantibodies, such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The gene discussed is FCGR2A; the disease is systemic lupus erythematosus.