TAMs create an immunosuppressive tumor microenvironment that further accelerates tumorigenesis by engaging different mechanisms such as: (i) activation of the immune checkpoint blockade, mainly involving programmed death ligand 1 (PD-L1) and programmed cell death protein 1 (PD-1), (ii) enhanced expression of enzymes hampering immune cell function (i.e., arginase 1) and (iii) by the release of anti-inflammatory cytokines [38,39]. Here, ARG1 is linked to neoplasm.