Portal hypertension is the most important complication that develops in patients with cirrhosis. Several studies have shown that angiogenesis (i.e. splanchnic neovascularization) driven by VEGF and other proangiogenic molecules, like PDGF, may be a major mechanism involved in portal hypertension, hyperdynamic splanchnic circulation and portosystemic collateralization. According with this, antiangiogenic therapies, like sorafenib or sunitinib, have been recently shown to reduce portosystemic collateral circulation, improve splanchnic hyperdynamics and decrease portal pressure in experimental model of portal hypertension. This effect was associated to a decrease in VEGF, PDGF expression and splanchnic neovascularization. In addition, these therapies were associated with a decrease in both splanchnic and intrahepatic inflammatory infiltrates, in hepatic stellate cell activation and in intrahepatic fibrosis. These data suggest that antiangiogenic therapies may therefore, by limiting liver fibrosis and inflammation in cirrhosis, prevent the occurrence of severe complications, such as portal hypertension and potentially liver cancer.