Specialized intestinal epithelium occurs more frequently at the gastroesophageal junction than previously anticipated. It can occur either within tongues of mucosa (short segment Barrett's) or just beneath a normal z-line (intestinal metaplasia at the gastroesophageal junction). Whether the etiopathogenesis and the natural history of these two conditions are the same is as yet unclear. The role of gastroesophageal reflux disease (GERD), Helicobacter pylori, and inflammation at the gastroesophageal junction in the pathogenesis of short segment Barrett's and intestinal metaplasia at the gastroesophageal junction needs to be carefully documented. Intestinal metaplasia at the gastroesophageal junction, short segment Barrett's, and Barrett's may represent a continuum of the same disease process. Recent evidence suggests, however, that short segment Barrett's shares similar characteristics with Barrett's but may be distinct from intestinal metaplasia at the gastroesophageal junction. It is conceivable that short segment Barrett's may remain steady or even regress if and when the noxious influence wanes but, with continuing stimulation, short segment Barrett's may lengthen further to become what we observe to be Barrett's. If correct, endogenous or exogenous factors that induce progression need to be identified. Acid and bile reflux and H. pylori are possible candidates acting either singly or synergistically. Finally, the true neoplastic potential of short segment Barrett's needs clarification.