Therefore, we examined the formation of inflammation-related DNA lesions (8-nitroguanine and 8-oxodG) and a stem cell marker (CD133) in biopsy specimens of BEA patients in comparison with those of normal esophagus and BE tissues for understanding the mechanisms of GERD-induced esophageal carcinogenesis. This evidence concerns the gene PROM1 and gastroesophageal reflux disease.