Under physiological conditions, macrophages are polarized into proinflammatory and antitumor M1 phenotype; however, tumor cells can switch macrophages to alternatively activated M2 phenotype via several pathways (CCL-2, IL-1, IL-4, IL-6, IL-8, IL-10, IL-13, CSF-1, PD-1/PD-L1, CD47/SIRPα, TGFβ) [5,7,8]. This evidence concerns the gene TGFB1 and neoplasm.