In conclusion, the CSF1/CSF1R axis could serve as an appealing target for MPE treatment because a) it repolarizes and depletes M2 macrophages, which are known to be the prevailing populations in MPEs and associated with dismal prognosis (23); b) it mediates stromal cell–M2 macrophage interactions that favor tumor progression and angiogenesis; c) both cell targets (macrophages and CAFs) are less prone to drug resistance because of their genomic stability (23, 46); and d) several CSF1R inhibitors are currently available showing a satisfactory safety profile (20). This evidence concerns the gene CSF1 and neoplasm.