Strategies to block the CD47–SIRPα axis include monoclonal antibodies targeting CD47 or SIRPα to disrupt their interaction [72,73,74]; engineered high-affinity SIRPα variants that enhance antibody-dependent phagocytosis [75,76], and gene- or nanotechnology-based approaches to downregulate CD47 expression on tumor cells [25] (Figure 1). The gene discussed is SIRPA; the disease is neoplasm.