Gastric precancerous lesions are a buzzword in gastroenterology. It includes gastroscopic intestinal epithelial metaplasia and heterogeneous hyperplasia. This pathological term is mainly associated with chronic atrophic gastritis and is an important stage in the transformation from normal gastric mucosa to gastric cancer. Since the etiology of gastric cancer is not fully understood, it is difficult to implement primary prevention against the etiology, therefore, the study of gastric precancerous lesions becomes one of the important elements of secondary prevention of gastric cancer. First of all, it should be clear that gastric precancerous lesions are based on atrophic gastritis, and with atrophic gastritis, it is not necessary to have enterosis and heterogeneous hyperplasia, but once enterosis and heterogeneous hyperplasia appear, the diagnosis of atrophic gastritis is clearly established. Second, intestinal epithelial hyperplasia is the replacement of epithelial cells of the gastric mucosa by intestinal epithelial cells, i.e., the appearance of epithelial cells in the gastric mucosa that resemble the mucosa of the small intestine or large intestine, which is a common lesion of the gastric mucosa and is seen in many chronic gastric diseases. The intestinal epithelial saprophytic cells are derived from undifferentiated cells in the neck of the gastric intrinsic glands, which are proliferation centers with the potential to differentiate into gastric and intestinal epithelial cells. Normally, it continuously differentiates into gastric-type epithelial cells to replenish the surface epithelium shed by senescence; in pathological conditions, it can differentiate into intestinal-type epithelial cells and form intestinal saprophytes. Intestinal epithelial metaplasia is divided into small intestinal metaplasia (i.e., complete intestinal epithelial metaplasia) and colonic metaplasia (i.e., incomplete intestinal epithelial metaplasia) by mucohistochemical staining. Small intestinal metaplasia, with good epithelial differentiation, is a common mucosal lesion and is widely seen in various benign gastric diseases (57.8%), especially in chronic gastritis, and the metaplasia increases with the development of inflammation, so it is thought that small intestinal metaplasia may belong to the nature of inflammatory reaction; while colonic metaplasia, with poor epithelial differentiation, has a low detection rate in benign gastric diseases (11.3%), but in the mucosa adjacent to intestinal gastric cancer The detection rate was very high (88.2%), indicating that colonic chemosis is closely related to the occurrence of gastric cancer. Generally, colon type chemosis occurs at a later age than small intestine type chemosis, and both are located in the more severe small intestine chemosis foci. The two types of chemosis can be mixed, so colon type chemosis may occur on the basis of the progressive aggravation of small intestine type chemosis. Thirdly, heterogeneous hyperplasia of gastric mucosal epithelium refers to a type of proliferative lesion in which the epithelium and glands of gastric mucosa deviate from normal differentiation and show heterogeneous morphology and function. It is generally believed that malignant tumors are almost always preceded by heterogeneous hyperplasia, and rarely transform from normal to malignant without going through this stage. Therefore, it is different from simple hyperplasia and tumorigenic hyperplasia. Simple hyperplasia is only the overgrowth of cells without obvious heterotypic cell structure, while tumorigenic hyperplasia is the autonomous growth of cells with obvious heterotypic cell structure. It should be said that heterogeneous hyperplasia is a junctional lesion between the two and is a true pre-cancerous lesion. Gastric mucosal epithelial heteroplasia occurs mainly on the basis of intestinalization, but also partly in the epithelium of the gastric pits. According to the degree and scope of differentiation of heterogeneous hyperplasia, it is classified into mild, moderate and severe, i.e. mild refers to inflammatory and regenerative benign heterogeneous lesions; moderate refers to heterogeneous lesions which are more obvious and close to the “critical lesions” of gastric cancer; severe refers to heterogeneous hyperplasia which is more obvious and morphologically difficult to be distinguished from differentiated cancer. However, it is often difficult to clearly distinguish between benign mild heterogeneous changes, critical heterogeneous hyperplasia, and malignant heterogeneous lesions because of the gradual migration and transformation process. Recent studies have further classified heterogeneous proliferations according to their tissue origin: 1) adenomatous heterogeneous proliferations: originating from intestinal epithelium, starting in the superficial mucosa, and becoming highly differentiated adenocarcinoma after carcinoma; 2) crypt-type heterogeneous proliferations: originating from the crypt, and becoming moderately or highly differentiated adenocarcinoma after carcinoma; 3) regenerative heterogeneous proliferations: seen in the regenerative epithelium of the mucosal defect, and becoming hypo- or undifferentiated adenocarcinoma after carcinoma. The regenerative heterogeneous proliferation is a dynamic process. Heterogeneous hyperplasia is a dynamic process that can progress from mild to severe, but it can also remain unchanged or be reversed, while severe heterogeneous hyperplasia is not easily reversed and can develop into gastric cancer. Therefore, severe heterotypic hyperplasia should be treated early. The clinical significance of heterotypic hyperplasia of gastric mucosa epithelium are: 1. Mild heterotypic hyperplasia: Mild heterotypic hyperplasia is an overproliferative response of mucosa to injury, often appearing at the edge of ulcer, or various types of gastritis, hyperplastic polyps, loss of protein gastropathy, etc., and is mostly regenerative in typology. Most of these lesions are reversible and do not require regular follow-up. 2.Moderate heterogeneous hyperplasia: The histological and cytological heterogeneity of moderate heterogeneous hyperplasia is more obvious and can appear in both atrophic gastritis, adenomatous polyps, etc., and also in the paracancerous mucosa. Although some cases are reversible or remain intact for a long time, some can evolve and escalate, so regular gastroscopic follow-up is required. 3.Severe heterogeneous hyperplasia: The histological and cytological heterogeneity of severe heterogeneous hyperplasia is obvious, and sometimes it is not easy to distinguish from highly differentiated carcinoma in the mucosa. This lesion is mainly seen in adenomatous polyps, peri-mucosa of cancer, occasionally just in the tumor foci themselves, with obvious malignant tendency and only little chance to reply to downgrade, so recent gastroscopic biopsy review and close follow-up observation should be done, and if cancer is suspected, surgical treatment should be performed, including gastroscopic polyp removal or laser cautery, debris-like polypectomy and surgical resection. Gastric precancerous lesions are not terrible, and it takes a long way for intestinalization and heterogeneous hyperplasia to develop into gastric cancer. It will not be more than about 5% of patients before they transform into gastric cancer. 5% is a statistically small probability event that can be considered almost never to happen, which is statistically based, so it is reasonable to think that intestinalization and heterogeneous hyperplasia are very safe and unnecessary to cause too much anxiety and worry. Also gastroscopic diagnosis under the naked eye and pathological diagnosis are often inconsistent. Since the field of view seen by the naked eye and pathology are different, the pathological diagnosis is the gold standard, but the pathological diagnosis is a very small area, and the rest depends on the gastroscopic diagnosis. It is very common that in a stomach, not all local lesions are the same, some are atrophic and some are not. But the place of intestinalization and heterogeneous hyperplasia must have started to atrophy. It needs to be brought to our attention.