Since the low rate of tumor-infiltrating immune cells, the development of lymphocyte exhaustion, and antigen insufficiency are common mechanisms that limit chimeric antigen receptor (CAR)-T cell therapeutic effectiveness (82), CAR-T cells engineered to deliver RIG-I/MDA5 agonists were able to restrict MDSC development by reducing their release of anti-inflammatory cytokines (e. g., TGF-β) and fostered DC subsets with costimulatory features, thus enhancing CAR-T cell efficacy in B16 melanoma-bearing mice, even when heterogeneous CAR antigen tumors lack adequate neoantigens (83). Here, TGFB1 is linked to neoplasm.