TAMs originate from myelomonocytic cells, and are recruited to the tumor microenvironment by tumor-derived cytokines and chemokines, including chemokine (C–C motif) ligand 2 (CCL2), vascular endothelial growth factor (VEGF), macrophage colony-stimulating factor (M-CSF), and transforming growth factor beta (TGF-β) [4, 5]. Here, TGFB1 is linked to neoplasm.