FcγRIIb-deficient mice exhibit loss of B cell self-tolerance at the IgG+ B cell and plasma cell stages, and development of SLE-like disease [24], demonstrating that FcγRIIb provides a distal peripheral checkpoint limiting the accumulation of self-reactive plasma cells and thereby preventing SLE. The gene discussed is FCGR2B; the disease is systemic lupus erythematosus.