We could speculate that metformin could be active in HCC either through mTOR (mammalian target of rapamycin) inhibition, or by interfering with the energetic balance of tumor cells by suppression of oxidative phosphorylation via AMPK (5’ adenosine monophosphate-activated protein kinase), consequently enhancing the efficiency of chemotherapy in p53-deficient cells [29,30]. Here, MTOR is linked to neoplasm.