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. This evidence concerns the gene ACSL4 and nasopharyngeal carcinoma.