Progression from liver damage (inflammation and cirrhosis) to HCC is linked to pathological new blood vessel formation, largely driven by vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2) pathway activation in endothelial cells, which disrupts the liver vascular architecture and induces the formation of portal-systemic collaterals and sinusoidal capillarization. This evidence concerns the gene VEGFA and hepatocellular carcinoma.