Given that negative regulators of ferroptosis such as nuclear factor erythroid 2-related factor 2, metallothionein-1G, and p53 confer resistance to sorafenib in HCC [8, 34], the discovery of a novel mechanism underlying ferroptosis induction is a promising therapeutic avenue to enhancing the antitumor efficacy of sorafenib against HCC. The gene discussed is MT1G; the disease is hepatocellular carcinoma.