In lenvatinib-resistant HCC cells, lactylation at K76 of IGF2BP3 upregulates the expression of PCK2 and NRF2 and restores redox homeostasis by increasing GSH and NADPH levels and reducing reactive oxygen species (ROS) production, thereby attenuating lenvatinib-induced apoptosis and promoting therapeutic resistance [74]. This evidence concerns the gene IGF2BP3 and hepatocellular carcinoma.