Metaplasia, wherein 1 type of adult tissue replaces another, is a consequence of chronic inflammation.1 Presumably, metaplasias develop and persist because they are more adept than the native tissue at resisting injury from the underlying inflammatory condition. In the stomach, intestinal metaplasia develops in the setting of chronic Helicobacter pylori gastritis, whereas intestinal metaplasia in the esophagus results from chronic esophagitis caused by gastroesophageal reflux disease (GERD). Limited dialogue between investigators studying intestinal metaplasia in the stomach and those studying it in the esophagus has been a barrier to progress in understanding these conditions.