To further support the role of Akt1 in HCC progression, a study demonstrated that the overexpression of myriostylated Akt1—and thus constitutively active Akt1—led to a liver tumor development in mice, and its combination with S-phase kinase-associated protein overexpression exacerbated the phenotype [25]. This evidence concerns the gene AKT1 and hepatocellular carcinoma.