Using monoclonal antibodies in a mouse model of ITP, Nieswandt and colleagues first demonstrated that removing the Fc fragment of anti-GPIbα monoclonal antibodies did not prevent thrombocytopenia, whereas the opposite was noted for anti-GPIIb/IIIa antibodies, denoting the Fc independence of anti-GPIbα antibodies in causing thrombocytopenia [82]. The gene discussed is ITGA2B; the disease is autoimmune thrombocytopenic purpura.