CTLA-4 inhibition combined with the “trimab” scheme (composed of immune activating anti-CD40 and anti-CD137 mAbs, a blocking antibody against the DR5 receptor for TNR-related apoptosis inducing ligand) substantially increased the tumor rejection rate of established mammary tumors in mice compared to trimab alone [126]. Here, TNFRSF9 is linked to neoplasm.