engineered hybrid cellular membrane nanovesicles, which were fused by three different cell derived NVs including platelet‐derived NVs (P‐NVs), M1‐like macrophage‐derived NVs (M1‐NVs), and cancer cell‐derived NVs with overexpression of high‐affinity SIRPα variants (SαV‐C‐NVs) (Figure 14).[252] Since P‐NVs can interact with circulating tumor cells (CTCs), M1‐NVs can reprogram tumor‐supportive TAMs into anti‐tumor M1 phenotype, and blocking CD47‐SIRPα axis can promote tumor‐phagocytosis of macrophages, the resultant hNVs inherit the properties of source cells. The gene discussed is SIRPA; the disease is neoplasm.