Similarly, a defect in FcγRIIB/SHIP pathway triggers an increased Ca2+ response, an increased activation of Erk2 and Akt pathways and also (for FcγRIIB) the spontaneous production of antinuclear autoantibodies associated with the development of glomerulonephritis (Bolland & Ravetch, 2000; Helgason et al, 2000; Liu et al, 1998; Takai et al, 1996). The gene discussed is INPP5D; the disease is glomerulonephritis.