Reflux of duodenal contents appears to contribute to the development of esophagitis and Barrett's adenocarcinoma [15,17] DCA-induced sustained AP-1 activation is likely to have important implications in esophageal tumorigenesis considering that blockage of DMBA (7,12-dimethylbenz [a]anthracene)/PMA-induced AP-1 activity in transgenic mice has been demonstrated to prevent neoplastic transformation in a murine keratinocyte model [22]. The gene discussed is FOS; the disease is esophagitis.