Disruption of the COX-2/PGE2 signalling has been successful in reducing MDSC recruitment and differentiation, repressing MDSC-associated suppressive factors such as ARG1 expression and ROS production, and shifting an inflammatory tumour profile to more anti-cancer immune rejection; consequently, COX-2 inhibition has resulted in improved CTL frequency and immune response, delayed tumour growth, and synergy between checkpoint inhibitors and dendritic cell-based immunotherapy [71,222,223,225,226]. Here, ARG1 is linked to neoplasm.