Gastroesophageal reflux disease is more frequent in post-gastrectomy patients than in normal subjects. Studies have found that nearly 1/3 of patients develop GERD after partial or total gastrectomy, and such reflux is one of the risk factors for esophageal cancer. In proximal gastrectomy, the anti-reflux effect of the cardia and lower esophagus sphincter no longer exists because of the removal of the cardia and lower esophagus, and the reflux of gastric acid from the stomach to the esophageal lumen causes anastomotic edema, inflammation, and even erosion of the anastomotic portion, which leads to the development of reflux esophagitis. This is mainly due to: (i) surgical removal of the cardia and ventral segment of the esophagus, destruction of mechanical anti-reflux structures such as the high-pressure zone and His angle in the lower part of the normal esophagus, and changes in the esophagogastric pressure gradient, making it easy for gastric contents to reflux into the esophagus. (ii) The severed vagus nerve stem and the removal of the gastric peristaltic pacing point in the upper part of the lateral greater curvature of the stomach resulted in the loss of the vagus nerve’s coordination of gastric peristaltic-type contractions, causing the disappearance of peristalsis in the body of the remnant stomach and the weakening of peristalsis in the sinus, resulting in delayed uncleared function. (3) The surgery removed the bottom of the stomach and part of the gastric body, leaving only the more acid-secreting gastric sinus, resulting in a significant reduction in the volume of the stomach and a decrease or absence of the accommodative relaxation effect of the stomach, leading to an increase in its pyloric pressure and an increase in the resistance to gastric emptying, thus making the acid-rich gastric contents flow back into the esophagus easily. Patients after major gastrectomy in the Bi-I style are prone to regurgitation of duodenal fluid into the remnant stomach and, likewise, into the esophagus because the pyloric sphincter is removed. In patients after Bi-II style gastrectomy, the proximal jejunum is anastomosed with the remnant stomach, and the duodenal fluid flows directly into the remnant stomach, which is also more likely to flow into the esophagus. Although gastric acid secretion is reduced in patients after major gastrectomy and acid reflux in the esophagus is not obvious, the prevalence of reflux esophagitis is higher in patients after major gastrectomy Bi-II than in the general population. The prevalence of reflux esophagitis was higher in patients after Bi-II surgery than in patients after Bi-Ⅰ surgery, which may be related to the reflux of duodenal fluid. The duodenal fluid contains bile and pancreatic juice, which, in concert with gastric acid and pepsin, aggravate the damage to mucosal epithelial cells, which may explain the higher prevalence of reflux esophagitis in patients after Bi Ⅰ surgery than in the general population, and the higher prevalence of reflux esophagitis in patients after Bi Ⅱ surgery than in patients after Bi Ⅰ surgery.