CCL2 and neoplasm: In the tumor microenvironment, a dominant and persistent STAT3 activity efficiently suppresses M1 macrophage polarization, dampening cytotoxic and proinflammatory functions (82) and favoring the accumulation of M2-polarized TAMs (83), that contributes to tumor immunoescape releasing pro-angiogenic molecules (e.g. VEGF, C-C motif chemokine ligand 2, CCL2), essential tumor-growing factors (e.g. epidermal growth factor, EGF), and immunosuppressive mediators (e.g. IL-10, transforming growth factor, TGF-β) (70, 76).