The molecular pathogenesis of HCC is multifactorial and is reliant upon dysregulation of multiple pathways including WNT/b-catenin, mitogen-activated protein kinase (MAPK), phosphatidylinositol-3 (PI3K)/AKT/mammalian target of rapamycin (mTOR), VEGF, PDGF, insulin-like growth factor (IGF), epidermal growth factor (EGF), TGF-beta, and hepatocyte growth factor [6, 7]. This evidence concerns the gene VEGFA and hepatocellular carcinoma.