Antibody-dependent cell-mediated phagocytosis (ADCP) is one of the important mechanisms of action for antibody drug development. FcγRIIa is the predominant Fcγ receptor involved in the ADCP process. FcγRIIa is expressed in myeloid effector cells, including macrophages and neutrophils, where it plays a role in the activation of these effector cells. Several clinical studies have studied the correlation of a FcγRIIa polymorphism (R131H) and the response to IgG1 subclass monoclonal antibodies (mAbs) such as rituximab. Engineered amino-acid substitutions in Fc-mAbs have been developed to enhance the mAb-mediated phagocytosis of tumor cells by macrophages.