Thus, using anti-mouse CTLA-4 mAbs with identical Fv but distinct isotypes of Fc, Selby et al. demonstrated that the ability of anti-mouse CTLA-4 mAbs to induce tumor rejection is determined by the Fc portion.16 Specifically, those with stronger affinity for activating FcgRs, including IgG2a and IgG2b can effectively induce tumor rejection and Treg depletion in the tumor microenvironment. The gene discussed is CTLA4; the disease is neoplasm.