Importantly, NDV’s viral proteins, notably the V protein, can later suppress IFN-β production in a biphasic pattern [85, 86].This dynamic modulation of type I IFN defines a critical therapeutic window for combining NDV with CAR-T cell therapy: early IFN-β activation primes the TME and enhances immune recruitment, while later suppression or upregulation of immune checkpoints requires precise timing of CAR-T cell infusion to maximize anti-tumor effects and avoid immunosuppressive feedback [87]. The gene discussed is IFNB1; the disease is neoplasm.