In other forms of human cancer, the overall abundance of TNFR2 Tregs is higher than in peripheral blood.13 Both murine and human data show that the unique TNFR2 target is preferentially expressed on Tregs and is a functional receptor—indeed, the master switch—for Treg survival.8 Tregs either die with TNFR2 blockade or expand with TNFR2 stimulation. Here, TNFRSF1B is linked to cancer.