They may include overexpression in tumor tissues of inhibitory receptor/ligands (e.g., PD-1/PD-L1); production by tumors of various soluble factors such as IL-10, TGF-β, IL-35, IDO, arginase, galectin 9, adenosine, COX-2, PGE2, and/or oxygen radicals; accumulation in the TME of metabolic alterations such as, e.g., glucose deprivation; enhanced activation of immune regulatory cells, e.g., Treg, myeloid derived suppressor cells (MDSC); the MHC class I down-regulation/loss or inactivation of β2-microglobulin on tumor cells; and other mechanisms of the immune evasion as previously reviewed [2,3]. Here, TGFB1 is linked to neoplasm.