Chronic DGR, wherein BAs abnormally reflux from the duodenum into the stomach, is another main risk factor in addition to Hp infection for the development of gastric IM and its progression to intestinal-type gastric adenocarcinoma.11,12 In this study, we found that exposure to DCA, as the predominant secondary BA in the stomach, activates a novel signaling axis comprising TGR5-STAT3-KLF5 in the gastric epithelium. The gene discussed is GPBAR1; the disease is gastric adenocarcinoma.