Elevated expression of HDLBP stabilizes lncFAL to decrease ferroptosis vulnerability by diminishing TRIM69-mediated FSP1 degradation in HCC cells.133 Inhibition of FSP1 enhances the antitumor activity of ferroptosis inducers, supporting the potential utility of targeting FSP1 as a therapeutic approach for HCC patients with high HDLBP or lncFAL expression.133. This evidence concerns the gene AIFM2 and hepatocellular carcinoma.