Given that macrophages are abundant in MC38 and PDA tumors12 and irradiation (IR)-induced damage-associated molecular patterns (DAMPs), such as HMGB1 and calreticulin (CRT), are able to activate phagocytes via TLR or LRP-1 signaling pathways13–15, we postulated that IR-induced DAMPs in the tumor microenvironment (TME) could stimulate Sirpα−/− macrophages to phagocytose tumor cells and thereby control tumor growth in Sirpα−/− mice. The gene discussed is SIRPA; the disease is neoplasm.