Liver steatosis/steatohepatitis can induce, in the absence of fibrosis, a haemodynamically significant increase in intrahepatic resistance due to both altered microvascular architecture and functional factors, such as blunted response to insulin dependent vasodilation, vasoconstrictors overproduction and endothelial dysfunction, the latter being involved at a very early stage of liver damage, even before the development of inflammation [44, 50, 51]. This evidence concerns the gene INS and endothelial dysfunction.