Shear stress, whose magnitude depends on the blood flow and the area of the intrahepatic sinusoids [71], physiologically drives Kruppel-like factor 2 (KLF2) transcription, which is responsible for NO production and is markedly increased in the liver of cirrhotic rats as negative feedback to counteract the vascular derangement occurring in advanced stage liver disease [72]. This evidence concerns the gene KLF2 and liver disorder.