However, in tumor microenvironments, tumor-mediated soluble factors, such as cytokines (IL-10, IL-6, TGF-β), enzymes (indoleamine 2,3-dioxygenase, arginase), and lipid mediators (prostaglandins), impair the phenotypic and functional properties of DCs and skew their differentiation by bone marrow precursors toward immunosuppressive and tolerogenic DCs (or regulatory DCs) [33,34]. This evidence concerns the gene TGFB1 and neoplasm.