In contrast, suppression of PI3K/Akt signaling transitions aerobic glycolysis to oxidative phosphorylation, accompanied by restored mitochondrial function, which indicates the involvement of PI3K/Akt signaling in metabolic reprogramming during HCC progression.275 In addition, inhibition of PI3K/Akt signaling elicits increased expression of caspase-3 and caspase-9, apoptotic markers, within HCC cells.276 Overall, these findings suggest the excitatory role of PI3K/Akt signaling in the evolution of HCC. Here, AKT1 is linked to hepatocellular carcinoma.