PARPi-induced remodeling of the tumor microenvironment can upregulate one or more of these pathways, providing a mechanistic rationale for combining phagocytic checkpoint blockade (for example, anti-CD47 or anti-SIRPα) or myeloid-reprogramming agents (including CSF1R, TREM2, or MerTK inhibitors), and potentially modulators of antigen-processing enzymes like Cathepsin S, to convert macrophage accumulation into effective antitumor immunity in prostate cancer (42). This evidence concerns the gene CD47 and neoplasm.