The pathophysiology of reflux esophagitis involves contact of the esophageal epithelium with acid-pepsin in the refluxate. For this contact to occur with sufficient duration, there must either be a combination of defects in antireflux and luminal clearance mechanisms for acid-pepsin to overwhelm a previously healthy epithelium or primary defects within the epithelium develop that subsequently enable 'normal' acid contact times to become damaging to the epithelium. This report examines these 2 pathways to reflux esophagitis and questions the causative role attributed to some phenomena. In either case, the final common pathway for the clinical expression of reflux esophagitis is by damage to the esophageal epithelium that is responsible for the development of heartburn and/or esophageal necrosis and inflammation.