ROS overproduction and subsequent diminished NO levels are responsible for a substantial decrease in the inhibition of thrombogenesis by dysfunctional LSECs; the attenuated expression of thrombomodulin, NO, and prostaglandin I2 is associated with the increased exposition of von Willebrand factor (vWF), integrins, and other receptors that cause clot formation by interacting with activated platelets [65,66], suggesting that liver fibrosis may result from microvascular thrombosis. Here, VWF is linked to Hepatic fibrosis.