Furthermore, because these RBCs were opsonized ex vivo, our data suggest that the function of 2A-2HC in ITP cannot solely be attributed to blockade of the FcRn, which has the potential to decrease the half-life of the MWReg30 anti-platelet antibody used in our ITP model [23]. The gene discussed is FCGRT; the disease is autoimmune thrombocytopenic purpura.