In ADCC—the primary MOA—tumor-bound anti-GD2 mAbs engage Fcγ receptors on the surface of NK cells and granulocytes, followed by the release from these cells of cytotoxic granules (serine proteases, or granzymes [specifically, granzyme B]) and cytokines (particularly perforin, a glycoprotein that creates pores in targeted cell membranes) (69), causing Fc-dependent phagocytosis and lysis of tumor cells (68, 70). The gene discussed is PRF1; the disease is neoplasm.