AKT1 and hepatocellular carcinoma: This phenomenon results in the PI3K-threonine kinase (AKT)—mechanistic target of rapamycin complex 1 (mTORC1)/β-catenin and NOTCH2 signaling pathways—being activated, triggering the expression of important effector molecules, such as BIRC5 and MYC proto-oncogene, which consequently promote the self-renewal of HCC cells [119].