In spite of these studies, the varying expression by different tumors of Fc receptor subclasses with their varying binding affinities, along with the potentially synergistic role of Fc-related effects and Hu5F9-G4 antibody therapy, our observed increase of GBM phagocytosis may be a shared contribution of tumor cell opsonization and the disruption of CD47-SIRPα interactions [41, 42]. The gene discussed is CD47; the disease is neoplasm.