Compatible with findings from earlier studies (15, 25), genetic or pharmacologic depletion of COX-2 and mPGES-1 similarly enabled the recruitment of the classic CD8a+ DC subset, which is essential in initiating CD8+ T-cell priming and directing, into the tumor site by suppressing PGE2 production and provoking type I IFN-mediated chemokines; however, this subset was also trafficked by anti-PD-1 monotherapy, probably because of IFNγ produced by drug-activated T cells (41), and no synergistic effect of mPGES-1 and COX-2 inhibitors was observed. This evidence concerns the gene CD8A and neoplasm.