OA has been shown to counteract the cytotoxic effects of lung cancer–targeting drugs in cell lines with activating epidermal growth factor receptor (EGFR) mutations [20]; meanwhile, OA can reduce syndecan 4 expression and facilitate ferroptosis in lung cancer cells via the glutathione peroxidase 4 (GPX4)/long‐chain acyl‐CoA synthetase (ACSL4) pathway, offering a strong rationale for employing ferroptosis‐targeting drugs in lung cancer therapy [23]. This evidence concerns the gene ACSL4 and lung cancer.