Mice deficient in SAP are resistant to experimental models of lupus (pristane-induced SLE and Murphy Roths Large (MRL)/lymphoproliferation (lpr) spontaneous SLE models), and this protection is attributed to impaired development of humoral immunity associated with defective germinal center formation and subsequently decreased antibody, including autoantibody, response (48, 49). The gene discussed is SH2D1A; the disease is systemic lupus erythematosus.