The functional characterization of the GITR-TGF-β network in co-culture experiments using glioma cells with syngeneic immune cells revealed that exposure to an agonistic GITR antibody in combination with a TGF-β inhibitor resulted in increased T cell activation, dominantly in the CD4+ T cell compartment (Fig. 2A). The gene discussed is TNFRSF18; the disease is central nervous system cancer.