This may be achieved using monoclonal antibodies (mAb) specific for cell surface molecules (CD25, Toll-like receptor, CTLA-4, GITR, OX40, and folate receptor 4) that are predominantly expressed by Tregs or specifically able to modulate Treg function.33 For instance, removal of Tregs by anti-CD25 mAb or toxin-conjugated anti-IL-2 (denileukin difitox) facilitates the activation and expansion of effector T cells that inhibit tumor growth in rodents. This evidence concerns the gene TNFRSF18 and neoplasm.