Scientific research has shown that a hostile tumor microenvironment can be significantly regulated by IL-12 through multiple mechanisms, including reactivation of anergic tumor-infiltrated lymphocytes (TILs), inhibition of Treg-mediated suppression of effector T cells, recruitment of NK cells to the tumor site, and inhibition of IL-10 and transforming growth factor-β (TGF-β) secretion by tumor-associated macrophages (TAM). The gene discussed is IL10; the disease is neoplasm.