We suggested that these compounds might disrupt the prototypical survival pathway known as AMPK/mTOR and BCL-2, which is becoming more and more associated with the development of HCC carcinogenesis [38, 40]; additionally, we assessed the simulated binding process toward AMP-activated protein kinase (AMPK)/mTOR and B-cell lymphoma 2 (BCL-2) as the molecular target for inhibition using molecular docking, and we employed quantitative PCR to analyze the genes expression. This evidence concerns the gene BCL2 and hepatocellular carcinoma.