This is a key step in hepatocarcinogenesis that is determined by an unbalanced angiogenesis process with an augmented production of proangiogenesis factors (drivers of vessel growth and maturation) by tumor cells and adjacent cells, including VEGF, platelet-derived growth factor (PDGF), placental growth factor, angiopoietins, hepatocyte growth factor, endoglin, transforming growth factor, basic fibroblast growth factor, and a diminished production of inhibitors such as angiostatin, endostatin, thrombospondin-1 [3,6,9]. This evidence concerns the gene FGF2 and neoplasm.