ACSL4 overexpression enhances ferroptosis resistance by preferentially incorporating polyunsaturated fatty acids (PUFAs) into phospholipid membranes [45], while ACSL1 suppression disrupts mitochondrial β-oxidation, forcing HCC cells to rely on glutamine anaplerosis—a vulnerability that may be targeted via glutaminase inhibition [46]. The gene discussed is ACSL1; the disease is hepatocellular carcinoma.