Tumor immune escape is closely related to the therapy resistance and it may be realized via the following mechanisms, involving TAMs: attraction of immunosupressive cells to the TME, (via CCL22 [61], TGF-β and IL-10 [62]) stimulation of effector T-cells exhaustion and dysfunction [63,64,65], expression of immunosuppressive molecules or their receptors, including programmed death-ligand 1/programmed death-1 (PD-L1/PD-1), LAG-3 and CTLA4, or ‘do-not eat me’ signal (CD47) on the surface of the tumor cells [62] that can inhibit the activation of effector T-cells. This evidence concerns the gene TGFB1 and neoplasm.