Recent studies have demonstrated that the therapeutic efficacy of anti-mouse Ctla-4 mAbs is affected by the Fc subclass and host Fc receptor, which in turn affect antibody-dependent depletion of Treg cells selectively within the tumor microenvironment.9–11 However, it has not been tested whether such depletion requires blockade of the B7-CTLA-4 interactions. The gene discussed is CTLA4; the disease is neoplasm.