Although many factors are involved in the pathogenesis of gastroesophageal reflux disease (GERD), the antireflux barrier at the gastroesophageal junction is the final determinate of reflux. In the majority of cases, transient lower esophageal sphincter (LES) relaxations appear to be the necessary condition for reflux to occur. In severe cases of GERD, especially those with esophagitis, stricture, and Barrett's epithelium, diminished resting LES pressure plays a contributory role. Esophageal dysmotility may be an additive factor leading to increased esophageal acid contact time and predispose patients to developing erosive esophagitis. Also, delayed gastric emptying may further compromise the LES. Finally, the role of bile reflux across an incompetent gastroduodenal (pyloric) junction remains controversial.