EGFR and neoplasm: For non‐small lung cancer cells, CD47 expression was upregulated in the cancer cells' resistance to EGFR inhibitor treatment, and CD47 blockade increased the clearance of the resistant cells by phagocytes.[19] Given that receptor tyrosine kinase‐targeted therapies are prevalent in treating many types of cancer, our findings elucidate a novel mechanism underlying CD47 expression in RTK‐activated tumor cells and underscore the synergetic tumor inhibition effect elicited by combined treatment with EGFR inhibitors and CD47‐SIRPα blockade.