The results were consistent with our in vitro study, where tmCRT/39-272 elevated TGF-β release, and the effects were reversed by anti-TGF-β antibody in vitro. Taken together, we conclude that tmCRT/39-272 activated the immune system and initiated the immune response at the early stage of tumor progression, and macrophages were activated and released a large amount of proinflammatory cytokines, contributing to the phagocytosis of tumor cells. Here, TGFB1 is linked to neoplasm.