The accumulation of genetic changes in an inflammatory milieu, along with the aberrant activation of oncogenic pathways, specifically Phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/protein kinase B (Akt) PI3K/AKT and mammalian target of rapamycin mTOR signaling, further promotes the progression to HCC [66]. Here, AKT1 is linked to hepatocellular carcinoma.