The injury of the esophageal epithelium may be determined by the reflux of the gastric acid in the esophagus. Barrett’s esophagus (BE) is characterized by the replacement of the normal squamous epithelium with the columnar epithelium, when the healing of the lesion occurs. According to some studies, the incidence of the esophageal adenocarcinoma in patients with BE is of about 0,5% per year.

The term Barrett’s esophagus is subjected to interpretation nowadays, so it lacks the clarity needed for the clinical and scientific communication on the subject of columnar metaplasia of the esophageal mucosa.

The major pathogenetic factor in the development of BE is represented by the reflux disease.

The cellular origin of BE is controversial and it represents an issue that needs to be resolved because it will have implications in the putative molecular mechanisms underlying the metaplastic process.

The epigenetic or genetic changes, which alter protein expression, function, and/ or activity, in post-mitotic cells to drive transdifferentiation or in stem/ progenitor cells such that they are reprogrammed to differentiate into columnar rather than squamous cells, are driven by the inflammatory environment created by chronic reflux.

In order to be able to develop better therapeutic strategies for the patients with this disease, an increasing interest in understanding the pathogenesis of BE at the cellular and molecular level presents these days.