A conundrum for exploitation of this mechanism in the setting of portal hypertension, however, resides in the fact that in liver cirrhosis an enhanced binding of eNOS to caveolin-1 [6–9,30,31], alters the post-translational handling of the protein in LSEC leading to impaired generation of NO (Fig 7), a mechanism that is deemed essential for development of portal hypertension in patients with liver cirrhosis [6–9,30–33]. This evidence concerns the gene CAV1 and cirrhosis of liver.