Alternatively, there are multiple strategies of reorienting rather than directly depleting TAMs for cancer therapy, which has recently been reviewed elsewhere [10, 11, 24], including targeting both the tumor cells (e.g., CD47 antibody) and the TAMs (e.g., CSF1/CSF1R blockades, TLR agonists, PI3Kγ inhibitors, CD40 agonists, and Class IIa histone deacetylase (HDAC) inhibitors). The gene discussed is CSF1R; the disease is neoplasm.