ADCC and ADCP are the most widely appreciated FcγR‐dependent effector functions (Figure 1a, b) and are, respectively, mediated primarily via  FcγRIIIa on NK cells and professional phagocytes such as macrophages. These effector functions, particularly NK cell ADCC, are believed to be major components of the MOA of cytotoxic therapeutic mAbs used in cancer therapy. In addition, ADCP can also occur via FcγRIIa and FcγRI,45 but the extent to which cytotoxic anticancer therapeutic mAbs depend on these for their MOA in patients is unclear. The improvement in clinical utility of mAbs engineered for selectively increased FcγRIII binding suggests that FcγRIIa and FcγRI may be less important in vivo in cell killing effects but perhaps are more important in other aspects of therapeutic efficacy—discussed later.