In clinical work, we often encounter patients who are very nervous because Barrett’s esophagus is found in gastroscopy. Most of the patients would check the introduction of Barrett’s esophagus on the internet and become frightened and anxious when they see that it is a precancerous lesion of esophageal cancer, as if they were patients of esophageal cancer. Perhaps people’s fear of certain things is often due to their lack of understanding or slight knowledge of it. When you get to know the person, the fear may be gone. Regarding Barrett’s esophagus, patients are often most concerned about what it is, how serious it is, and whether esophageal cancer can occur. Here we can get to know Barrett’s esophagus with you. Barrett’s esophagus is a pathological phenomenon in which the compound squamous epithelium of the lower esophagus is replaced by a single layer of columnar epithelium with or without intestinalization. Those with intestinal epithelial metaplasia are precancerous lesions of esophageal adenocarcinoma. It is still controversial whether those without intestinal metaplasia are precancerous lesions or not. It is closely related to the development of esophageal cancer and is a major precancerous lesion of esophageal adenocarcinoma. The etiology of this disease is unknown; initially, this change was thought to be caused by congenital short esophagus, but later it was proposed to be due to the repair process of reflux esophagitis. Clinically, it is mostly secondary to gastroesophageal reflux disease and esophageal hiatal hernia. Various components of the reflux, including acidic gastric juice, alkaline bile, and pancreatic juice, can cause damage to the squamous epithelium of the lower esophagus, which is repaired by the more acid-resistant and regenerative columnar epithelium, resulting in the formation of Barrett’s esophagus. Barrett’s esophagus (Reba’s esophagus) itself does not produce symptoms, and symptoms appear mostly due to esophagitis, ulcers, and strictures. It typically presents with symptoms of gastroesophageal reflux disease (GERD), such as heartburn, acid reflux, retrosternal pain, and difficulty swallowing. The main clinical significance of Barrett’s esophagus is currently considered to be its association with esophageal adenocarcinoma. Routine screening for Barrett’s esophagus is not recommended for the general population and patients with GERD alone, but should be performed in those patients with multiple other risk factors (age 50 years or older, long-term reflux esophageal disease, diaphragmatic hernia, and obesity, especially abdominal obesity). The diagnosis of this disease is based mainly on endoscopy and esophageal mucosal biopsy. The diagnosis of Barrett’s esophagus can be made when the presence of columnar epithelial hyperplasia in the lower esophagus is detected by endoscopy and the presence of columnar cells is confirmed by pathological examination. Given the risk of BE developing into esophageal adenocarcinoma, and since early detection of malignancy improves patient survival, all guidelines recommend that patients with BE receive endoscopic follow-up surveillance, so patients with BE should be followed up regularly for early detection of heterogeneous hyperplasia and carcinoma. The interval of endoscopy should depend on the degree of heterogeneous hyperplasia. If no heterogeneous hyperplasia or early cancer is detected after 2 examinations, the interval between examinations can be relaxed to 3 years. For those with mild heterogeneous hyperplasia, endoscopic review should be performed once every 6 months in the first year, and if the heterogeneous hyperplasia does not progress, the review can be performed once a year. For BE with severe heterogeneous hyperplasia, there are two options: endoscopic or surgical treatment is recommended, or close monitoring follow-up with gastroscopy review every 3 months until detection of intramucosal cancer. The principles of treatment are to control gastroesophageal reflux, eliminate symptoms, and prevent and treat complications, including heterogeneous hyperplasia and carcinoma. Acid suppression therapy: Acid suppressants are the main drugs used to treat reflux symptoms. Endoscopic treatment: The commonly used endoscopic treatment methods include argon plasma coagulation, high-frequency electrical therapy, laser therapy, radiofrequency ablation, endoscopic mucosal resection and cryoablation. For BE without heterogeneous hyperplasia, endoscopic treatment is not advocated because of its low probability of cancer. BE with mild heterogeneous hyperplasia also has a low probability of carcinoma, so endoscopic follow-up can be performed first, and if it progresses to severe heterogeneous hyperplasia, endoscopic treatment should be performed. Surgical treatment: In principle, BE patients with proven cancer should be treated surgically. Anti-reflux surgery: including surgical and endoscopic anti-reflux surgery.