The most common hepatic consequence of jejunoileal bypass for morbid obesity is triglyceride accumulation (steatosis), which usually appears to be maximal during the period of acute weight loss. In certain patients, however, because of unknown factors such as the degree of steatosis, its duration, or an as yet undefined unusual patient susceptibility, probably of a metabolic nature, a chain of events is initiated which produces inflammation and fibrosis, culminating in cirrhosis. Certain analogies with alcohol-induced steatosis and its consequences are possible. Given differences between the two states for increased intracellular hepatocyte redox potential and possibly different predominant sources for fatty acid mobilization and production affecting increased intracellular triglyceride synthesis, the remainder of the pathway proposed for the development of cirrhosis from ethanolic liver disease may equally apply to the cirrhosis seen in postbypass patients. This complication, although rare (approximately 3%), has been the subject recently of more frequent reports, with death or near-death from hepatic failure. Suggested studies are indicated to support or refute the hypotheses put forward here.