This behaviour may be explained by the critical function of AMPK as a metabolic sensor and regulation of cell growth [76]; besides, AMPK negatively regulates the mTOR signal pathway, resulting in the inhibition of cancer proliferation and growth [77]; by incorporating signals from the PI3K/Akt pathway [11], it controls cell survival, proliferation, and angiogenesis [78]; additionally, HCC typically has elevated mTOR, which is linked to an early recurrence and a worse prognosis [79]; treatment for HCC has been proposed as the inactivation of mTOR to limit cancer cell growth [80]. Here, AKT1 is linked to hepatocellular carcinoma.