Although the mechanisms of action of IVIG have not been completely elucidated, the results from the clinical trial of GMA161, an anti-CD16 antibody that has shown efficacy on thrombocytopenia improvement in ITP patients [5], suggest that blockade of FcγRs is a possible mechanism of IVIG action. The gene discussed is FCGR3A; the disease is autoimmune thrombocytopenic purpura.