In summary, our findings on the effect of the FcγRIIIA p.159 polymorphism in PTLD suggest a genetic risk factor for PTLD, mediated through higher doses of immunosuppression; a reduced role of ADCC as a rituximab effector mechanism in the posttransplant setting; and competition between ADCC and other rituximab effector mechanisms in vivo. The gene discussed is FCGR3A; the disease is post-transplant lymphoproliferative disease.