Preclinical studies showed that the COX-2/mPGES1 pathway is able to promote tumor immune escape mechanisms by increasing the number of T regulatory cells [46] and myeloid derived suppressor cells [47], as well as by driving increased expression of indoleamine 2,3-dioxygenase 1 [48] and PD-L1 [24,49,50] by cancer cells. Here, PTGES is linked to neoplasm.