In vitro and in vivo mode-of-action studies provide strong evidence for Fc:FcgR-dependent antitumor mechanisms, e.g., macrophage-mediated antibody-dependent cellular phagocytosis and FcγR cross-linking-induced antibody tumor programed cell death, underlying BI-505’s therapeutic activity [16]. The gene discussed is FCGR2A; the disease is neoplasm.