Tregs aid in tumoral escape from immunosurveillance by mediating the various suppressing mechanisms: (1) the IL-2 receptors on Tregs bind to the surrounding IL-2 to reduce IL-2 availability for effector T cells, thus depriving their anti-tumor activities; (2) the constitutive expression of CTLA-4 on Tregs competitively binds to CD80/86 ligands on DCs, preventing them from activating CD8+ effector T cells [109]. Here, CTLA4 is linked to neoplasm.