By engaging SIRPα, CD47 limits the ability of macrophages to engulf tumor cells, which acts as a major phagocytic barrier.163 Based on this finding, exosomes designed to harbor SIRPα variants could function as immune checkpoint blockade that antagonizes the interaction between CD47 and SIRPα thus induce augmented tumor phagocytosis, leading to prime effective anti‐tumor T cell response163 (Figure 6a). The gene discussed is CD47; the disease is neoplasm.