Basically, the abrogation of MDSC migration inside tumor are based on antagonist antibodies for specific chemokine receptors [i.e., CXCR2 (192); CCR5 (193)] or small molecules [i.e., CXCR4 (194)]; on the contrary, strategies targeting the immunosuppressive functions of MDSCs are based on specific pharmacological inhibitors abrogating the activity of transcriptional factors [i.e., STAT3 (31)] or key immunosuppressive-associated enzymes [i.e., COX-2 (82)], as well as on checkpoint inhibitors [i.e., PD-1L (85)]. Here, PTGS2 is linked to neoplasm.