Hence, despite the GITR agonist antibody DTA-1 could overcome self-tolerance and reverse Treg suppression, secondary melanoma challenge tumors cannot be rejected during the early stages of primary tumor growth, unless Treg are depleted [40], indicating that the clinical consequence of an immune response might even depend on the ratio of effector vs regulatory T cells. The gene discussed is TNFRSF18; the disease is neoplasm.