AKT1 and hepatocellular carcinoma: In HeG2, Bel-7402, and SMMC-7721 hepatocellular carcinoma cells, RES inhibited the viability and proliferation of cancer cells and increased the apoptosis in a dose-dependent manner (20–200 μmol/L) via SIRT1 activation and concomitant inhibition of SIRT1-mediated post-translational modification of PI3K/AKT signaling [91].