Indeed, we found ectopic overexpression of a constitutive active form of AKT in Lenvatinib sensitive HCC cells promotes cell resistance to Lenvatinib treatment (Fig. 4), while depletion of AKT in Lenvatinib resistant HCC cells restored sensitivity to Lenvatinib treatment (Fig. 5). This evidence concerns the gene AKT1 and hepatocellular carcinoma.