As for OLE, treatment of HepG2 human hepatoma cells inhibited cell viability and induced apoptosis (upregulation of BAX and downregulation of Bcl-2), through activation of the caspase pathway and the modulation of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, suppressing the expression of activated AKT [175]. The gene discussed is AKT1; the disease is hepatocellular carcinoma.