Taken together, despite being derived from a limited set of assays, our findings provide evidence that, mechanistically, the synergistic anti-tumor effects of the high-order combination of OHSV2-DSTEFAP5/CD3, CAR-T cells, and immunotoxins, are likely involved in the functions of OHSV2-DSTEFAP5/CD3 to prime CD3+ T-cell activation and enhance proliferation of CD4+ and CD8+ T cells and even disrupt the entangled relationship between cancer cells and fibroblasts. The gene discussed is CD8A; the disease is cancer.