Fatty liver often has a benign course and is readily reversible with discontinuation of alcohol (or no more than one glass of wine per day, which has been reported in some, but not other, studies to reduce the frequency of NASH in persons with NAFLD), or treatment of other underlying conditions; if untreated, fibrosis progresses at an average rate of 1 stage every 14 years, with 20% of patients progressing more rapidly. In patients with NAFLD, the likelihood of NASH is increased by the following factors: obesity, older age, non–African American ethnicity, female sex, diabetes mellitus, hypertension, higher ALT or AST level, higher AST/ALT ratio, low platelet count, elevated fasting C-peptide level, and a high ultrasound steatosis score. NASH may be associated with hepatic fibrosis in 40% of cases with progression at a rate of 1 stage every 7 years; cirrhosis develops in 9–25%; and decompensated cirrhosis occurs in 30–50% of cirrhotic patients over 10 years. The course may be more aggressive in diabetic persons than in nondiabetic persons. Risk factors for fibrosis in patients with fatty liver without NASH are severe steatosis and the I148M variant of the PNPLA3 gene. Mortality is increased in patients with NAFLD, correlates with fibrosis stage, and is more likely to be the result of malignancy (including hepatocellular carcinoma, colorectal cancer, and breast cancer) and cardiovascular disease than liver disease. Risk factors for mortality are older age, male sex, white race, smoking, higher body mass index, hypertension, diabetes mellitus, and cirrhosis. Prognostic biomarkers are under study. Steatosis is a cofactor for the progression of fibrosis in patients with other causes of chronic liver disease, such as hepatitis C. Hepatocellular carcinoma is a complication of cirrhosis caused by NASH, as it is for other causes of cirrhosis, and has been reported even in the absence of cirrhosis. NASH accounts for a substantial percentage of cases labeled as cryptogenic cirrhosis and can recur following liver transplantation. Central obesity is an independent risk factor for death from cirrhosis of any cause.