Agonist mAbs directed against the co-stimulatory molecules, OX40 (CD134), glucocorticoid-induced TNF-related protein (GITR), and 4-1BB (CD137), have been used to boost antitumor T-cell functions, whereas blocking mAbs for the co-inhibitory molecules cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) and PD-1 have been employed to prevent a negative regulation of tumor-specific T cells (Figure 1). The gene discussed is TNFRSF4; the disease is neoplasm.