Tumor cells are able to escape immunosurveillancethrough severaldistinct mechanisms, one of which is the upregulation of the CD47anti-phagocytic signal.1 CD47 is a transmembraneprotein overexpressed by acute myeloid leukemia (AML) and severaltypes of solid tumors.2 The binding ofCD47 to its receptor signal regulatory protein α (SIRPα)on macrophages serves as a signal inhibiting the phagocytosis of tumorcells. This evidence concerns the gene CD47 and neoplasm.