Fox3z regulatory T cells are common in tumor microenvironment, where they induce immune-suppression. They do so by producing various cytokines, including TGF-b, IL-10, and IL-9, thereby promoting tumor growth. It was also shown that Treg secrete IL-35. IL-35 functions through IL-35R on various cell types, and is a potent immune-suppressor. Indeed, Treg-derived IL-35 was shown to inhibit antitumor T cell response, whereas IL-35-deficient Treg have significantly reduced activity in vitro and in vivo. Stable expression of EBI3, a gene that codes for IL-35 subunit, confers growth-promoting activity in lung cancer, whereas small interfering RNA silencing of EBI3 inhibits proliferation of lung cancer. Recently Wang et al. generated IL-35 producing plasmacytoma cancer cells and showed that the expression of IL-35 in tumor microenvironment GDC-0199 increased the number of myeloid derived suppressor cells, and promoted tumor angiogenesis; furthermore, IL-35 inhibited the infiltration of cytotoxic T lymphocytes into the tumor microenvironment and rendered the cancer cells less susceptible to CTL destruction. These experimental results suggest that blocking IL-35 may be an effective therapeutic approach to human cancer. To explore this possibility we develop in the present paper a mathematical model and then conduct in silica experiments to evaluate to what extend blocking IL-35 reduces tumor growth. The model consists of a system of partial differential equations that involve interactions among cells and cytokines. We first consider the situation which corresponds to the experiments in Wang et al.. In these experiments two kinds of plasmacytoma cells were injected into wild type mice: tumor cells that have been transfected with IL-35 so that tumor secretes high amount of IL-35 into the microenvironment, and “normal” plasmacytoma cells that secrete very small amount of IL-35. There is also a small amount of IL-35 produced by MDSC as well as IL-35 produced by Treg. We show that the model simulations agree with the experimental data in. We also introduce, in this model, the effect of a drug which inhibits production of IL-35, and simulate various protocols for administering the drug. We find, that administering the drug frequently in small amounts yields better results than administering it infrequently in larger amounts. We also find that the percentage of tumor reduction under anti-IL-35 drug improves when the production of IL-35 by cancer is increased. IL-35 is the most anti-inflammatory cytokine within the IL-12 cytokine family. In this paper we addressed the questions to what extend IL-35 is involved in tumor microenvironment and how effective is anti-IL-35 drug in reducing tumor growth. It is well known that Tregs are presented in the tumor microenvironment and that they secrete IL-35 to promote tumor growth.