In clinical work, many patients consult about the pathology report after gastroscopy, and it is necessary to popularize the knowledge of precancerous lesions of esophagus. Precancerous lesions refer to those that are directly related to the occurrence of tumor and histologically found evidence of its evolution into cancer, which can be stable and unchanged for a long time, or progress in two directions: improvement (cure) and malignant carcinoma. Squamous cell papilloma Although human papillomavirus (HPV) DNA has been found in papilloma and squamous carcinoma, and animal studies have confirmed that squamous cell papilloma is a precancerous lesion, especially HPV subtypes 16 and 18, it is rare in humans, being located in the distal esophagus, and in some cases may be multiple, with many patients having esophageal hiatal hernia, reflux esophagitis and peptic ulcer. However, atypical hyperplasia and carcinoma due to papilloma have not been confirmed in humans. Adenomas are usually solitary or multiple. 5/16 of Barrett’s esophagus patients with adenocarcinoma have a combination of adenomas that are associated with cancerous tissue. The immature cells that make up adenomas resemble atypical hyperplasia, which is rare in the esophagus. The difference between adenomas and atypical hyperplasia is that: (1) adenomas are tumors and are irreversible, whereas flat columnar epithelial atypical hyperplasia is reversible and its cells show varying degrees of abnormality; (2) adenomas have well-defined and nodular borders, and some adenomas have distinct contours and nests of carcinoma, whereas atypical hyperplasia has none of these features. Atypical hyperplasia Squamous epithelial atypical hyperplasia: atypical hyperplasia is common in tissues around esophageal cancer, and histology classifies atypical hyperplasia into mild, moderate and severe. In China’s high prevalence area, atypical hyperplasia is seen next to 66.7% of early esophageal cancers, and atypical hyperplasia is seen in 20% of esophageal cancers reported in Japan. The severity of atypical hyperplasia is inversely correlated with tumor infiltration, which is related to the development of tumor, so that the lesions are combined. Although atypical hyperplasia is reversible, definite severe atypical hyperplastic epithelium should currently be treated as esophageal cancer. Death from esophageal cancer within 30 years has been reported in 50% of those with severe atypical hyperplasia of the esophagus. Barrett’s epithelial atypia: Recent studies have shown that Barrett’s epithelium may predispose to esophageal adenocarcinoma, and follow-up studies have shown that the incidence of adenocarcinoma in Barrett’s esophagus varies between 1 in 52 and 1 in 81 case years, with a mean of 1 in 76 case years. Adenocarcinoma is usually associated with atypical hyperplasia of Barrett’s epithelium and is more common in intestinal epithelium and less common in gastric epithelium. The atypical hyperplasia of Barrett’s epithelium is divided into two types: low and high, where high includes moderate and severe atypical hyperplasia, and low is mild atypical hyperplasia. Among them, severe atypical hyperplasia should also be treated as esophageal cancer.