Activation of Pparα, which we have also seen in our study, has been shown to improve steatosis, inflammation and fibrosis in models of non-alcoholic fatty liver disease and Pparα agonists,(41) such as fibrates, have been reported to improve fatty acid oxidation in mice.(55) Furthermore, Pparα activation stimulates fatty acid and TG metabolism,(49) thereby decreasing hepatic TG levels. The gene discussed is PPARA; the disease is steatosis.