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Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder and is associated with metabolic dysfunction. Persistent hepatic inflammation in diseased livers results in progressive fibrosis and loss of hepatic function. Vascular adhesion protein-1 (VAP-1) is expressed on the hepatic endothelium and recruits leukocytes to the liver; however, it is also produced as a soluble form (sVAP-1) that has monoamine oxidase activity. In this episode, David Adams, Chris Weston, and Emma Shepherd discuss their work, which links sVAP-1 levels in patient serum to NAFLD severity and prognosis. In murine hepatic injury models, loss of VAP-1 or inhibition of VAP-1 enzymatic function reduced inflammatory cell recruitment to the liver and fibrosis. The results of this study suggest that targeting VAP-1 has potential as a therapeutic strategy for limiting hepatic inflammation and fibrosis.