Combination of entinostat with immune checkpoint inhibitors have resulted in prolonged survival, expansion of CD8+ T cells, and inhibition of immunosuppressive functions in both M-MDSC and PMN-MDSC via downregulation of ARG1, iNOS, and COX-2; overall, this resulted in a shift of the tumour dynamic into a more immune-susceptible TME [244,245]. Here, PTGS2 is linked to neoplasm.