This worked synergistically with co-administration of CTLA-4, but not with CD25 mAb (Ko et al., 2005) reinforcing the hypothesis that while both GITR and CD25 mAb inhibit Treg-mediated suppressor activity as a primary mechanism of promoting tumor immunity, CTLA-4 mAb independently contributes to tumor rejection by directly acting on effector T cells. Here, TNFRSF18 is linked to neoplasm.