A similar expression pattern has been demonstrated for CTSE in normal, metaplastic, dysplastic, and neoplastic gastric epithelium as well as in the intestinal dysplasia–neoplasia sequence in APCmin/+ mice.11–15 One explanation for our observed CTSE overexpression is that exposure to gastric refluxate induces expression of gastric proteases; consistent with this we found that despite the remarkable induction in BE tissues, CTSE levels are still lower than those found in either gastric fundus or cardiac mucosa. The gene discussed is CTSE; the disease is Barrett esophagus.