Concurrently, CSCs maintain tumor heterogeneity and promote growth through the upregulation of anti-apoptotic proteins, inhibition of death receptors (Fas/TRAIL-R), activation of the NRF2-KEAP1 antioxidant pathway, and autophagy, thereby evading apoptotic signaling and resisting DNA damage induced by radiotherapy, ultimately resulting in tumor resistance and recurrence [89,90]. The gene discussed is KEAP1; the disease is neoplasm.