In the same colon cancer model, as well as in 4T1 breast cancers, the combination of a TNFR2-blocking mAb with an immune stimulator (toll-like receptor agonist) markedly enhanced the antitumor efficacy of immunotherapy by reducing the number of tumor-infiltrating TNFR2+ Tregs and increasing the number of IFN-γ-producing CD8+ cells (Nie et al., 2018). Here, TNFRSF1B is linked to neoplasm.