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Effective immunotherapy requires tumor-specific CTLs to infiltrate the tumor and kill their target in situ. Although no clinical advantage was derived by the presence of tumor-specific CTLs in the peripheral blood in melanoma patients (40), their frequency in the tumor correlated with a favorable prognosis (41). These clinical observations seem to be confirmed in our model where sildenafil treatment (a) increased the CD8+ T cell tumor infiltration (Fig. 4 B) and (b) increased the percentage of activated T cells (Fig. 4, C and D). Moreover, the number of tumor-infiltrating T cells directly correlated with a measurable antitumor effect (Fig. 3). Extensive data exist in mouse models correlating tumor progression with the accumulation of myeloid inhibitory cells such as CD11b+/Gr-1+ myeloid-derived suppressor cells (MDSCs) (4), immature dendritic cells (5), and F4/80+ macrophages (6) that induce local and possibly systemic immunosuppression (7). L-Arginine metabolism is an important pathway used by MDSCs to blunt antitumor immunity (8). In these cells, arginase-1 (ARG1) and nitric oxide synthase�2 (NOS2), the key enzymes in L-arginine catabolism, work either alone or synergistically to suppress T cell function (9). The elimination, functional inhibition, or differentiation of MDSCs in tumor-bearing hosts can restore CD8+ T cell responsiveness (10, 11), thereby implicating their role in tumor-induced immunosuppression.