ACSL4 acetylation as a radiosensitizing mechanism is supported by robust biochemical and in vivo data; however, the contribution of broader lipid metabolic rewiring (e.g., PCK2 or P4HA1–HMGCS1 signaling) to clinical ferroptosis phenotypes in NPC remains more speculative and awaits translational correlation. The gene discussed is P4HA1; the disease is nasopharyngeal carcinoma.