IFNG and neoplasm: In the first model, blocking EP2 reprograms monocytic MDSC towards a NOS2low/TNFαhigh phenotype and restores anti-tumoral efficacy of IFNγ [84], while in the second one, PGE2 synthesis inhibitor limits secretion of protumoral cytokines and growth factors by bone marrow-derived mononuclear cells and thereby stimulates tumor destruction by T cells [85].