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A greater understanding of the role of MDSCs in tumor-induced immune dysfunction (7, 42) will establish the scientific rationale for a targeted pharmacologic approach to disrupt these suppressive mechanisms and may serve as an adjunct to immunotherapy. We previously showed that nitroaspirin could abrogate the inhibitory activity of MDSCs by enhancing the preventive and therapeutic efficacy of antitumor vaccines (43). However, despite its use as a vaccine adjuvant, nitroaspirin demonstrated no antitumor efficacy when used alone. In contrast, down-modulation of both ARG1 and NOS2 in MDSCs (Fig. 6) with PDE5 inhibitors effectively abrogates MDSC-mediated immune suppression, resulting in a measurable antitumor response (Fig. 1, Fig. 3, and Fig. 4). We have recently shown that to effectively exert their suppressive function, MDSCs must (a) be activated by IFN- production from antigen-stimulated T cells, (b) release their own IFN-, and (c) be responsive to IL-13 (29). 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