We show that the hNVs, which inherit the capabilities from source cells, can efficiently accumulate in surgical wound sites, interact with CTCs in the blood, repolarize TAMs towards M1 phenotype, and block the CD47-SIRPα interaction (Fig. 1b), thus accentuating macrophage phagocytosis of cancer cells, as well as potentiating antitumor T cell immunity, while reducing side effects induced by systemic infusion. This evidence concerns the gene CD47 and cancer.