Particularly given that ATR inhibitors (e.g., AZD6738) can enhance the radiosensitivity of HNSCC cells[36], exploring the combination of these inhibitors with standard chemoradiotherapy in SASH1-high patients, especially in p53-deficient tumors, represents a highly promising direction for overcoming therapeutic resistance[37]. The gene discussed is SASH1; the disease is head and neck squamous cell carcinoma.