The contribution of FcγR-mediated effector functions to the pathogenesis of ITP triggered by opsonized platelets has identified an association with reduced expression levels or impaired signaling of inhibitory FcγRIIB (326, 327) as well as the presence of a functional copy of the activating FcγRIIC gene (328). Here, FCGR2A is linked to autoimmune thrombocytopenic purpura.