Triptolide treatment significantly suppresses PD-L1 expression in oral squamous cell carcinoma and NSCLC, modulating the immune checkpoint response and effectively inhibiting tumor growth in PDTX models and an IFN-γ-modulated environment, while its combination with IFN-γ in locoregional treatment enhances antitumor immunity in triple negative breast cancer by reversing IFN-γ-induced PD-L1 expression and activating cytotoxic CD8+ T lymphocytes, resulting in synergistic tumor growth inhibition [982–984]. The gene discussed is IFNG; the disease is neoplasm.