While the role of glycolysis on AKT-dependent HCC development requires further investigation, the importance of lipogenesis in AKT-driven hepatocarcinogenesis has been underlined by a previous report from our group, in which depletion of FASN, the master regulator of fatty acid biosynthesis, completely abolished AKT-induced HCC development [30, 31]. The gene discussed is AKT1; the disease is hepatocellular carcinoma.