New insights into genetic predisposition and novel therapeutic targets for nonalcoholic fatty liver disease

Nonalcoholic fatty liver disease (NAFLD) is the most prevalent etiology of abnormal liver enzyme tests in the United States (1). The term NAFLD ranges from the relatively benign nonalcoholic fatty liver (NAFL) to the aggressive nonalcoholic steatohepatitis (NASH) to fibrosis and eventually cirrhosis, in the absence of excessive alcohol consumption (2). NAFL is defined as the presence of at least 5% hepatic steatosis (HS) without evidence of hepatocellular injury or fibrosis. NASH is defined as the presence of HS with inflammation and hepatocyte injury such as ballooning, with or without liver fibrosis (3). By the year 2020, NASH is anticipated to be the most common indication for liver transplantation among adults in the USA (4)