The observed dual activity of anti-CTLA-4 mAbs relies not only upon higher expression of the target molecule on Treg relative to Teff cells at the tumor site but also upon antibody isotype and enrichment of Fc-gamma receptor (FcγR)-expressing innate effector cell subsets with capacity for ADCC within the tumor microenvironment (Simpson et al., 2013). The gene discussed is FCGR2A; the disease is neoplasm.