AGT and Hepatic fibrosis: If NOX does not seem to play a direct role in modulating the intrahepatic vascular tone in cirrhosis, as its inhibition mediated by apocynin cannot reduce liver fibrosis [59], many studies point out NOX isoform upregulation as responsible for ROS increased production leading to hepatic fibrosis [60,61,62], and someone went even further, demonstrating that Angiotensin II—another key player in ED development—may be responsible for NOX upregulation, leading to HSC activation and ROS increased levels [63,64].