What is the relationship between eradication of HP infection and prevention of cancer in atrophic gastritis? It is generally believed that eradication of HP can effectively treat non-atrophic gastritis and prevent the progression of atrophy and intestinal metaplasia. Studies conducted in Changle, Fujian, a region with a high incidence of gastric cancer, have shown that eradication therapy can prevent gastric cancer in those without precancerous lesions at the time of HP eradication. Western medicine believes that there is an “irreversible point” in the progression of atrophic gastritis, and once this point is crossed, eradication will not be effective in preventing the progression of atrophic gastritis to gastric cancer. What are the ingredients in food that can help atrophic gastritis? Biologically active food components have a role in the prevention of gastric cancer such as antioxidant vitamins and selenium may reduce the risk of gastric cancer. Folic acid provides a one-carbon group that is necessary for DNA synthesis and has hypomethylation changes in carcinogenesis, so supplementation may improve atrophic gastritis and prevent gastric cancer from developing. The word intestinalization is often found in gastroscopy reports, and many people are confused as to what intestinalization means and what significance it has. Gastric mucosal atrophy can be divided into two types, one is saprophytic atrophy, which refers to the replacement of intrinsic gastric glands by saprophytic or pseudopyloric glands. The other type of atrophy is non-chemotropic atrophy, in which the intrinsic glands are replaced by fibrous or fibromuscular tissue, or the number of intrinsic glands is reduced due to inflammatory cell infiltration. What is commonly known as intestinalization is the replacement of gastric mucosal atrophy by intestinal glandular metaplasia. If the inflammation continues to evolve, the cell growth is atypical, i.e., heterogeneous hyperplasia (atypical hyperplasia, intraepithelial neoplasia); or even cellular hyperplasia leading to carcinogenesis. Mucus staining can be used to classify intestinal metaplasia; small intestine and complete intestinal metaplasia subtypes are not significantly related to gastric cancer, while large intestine metaplasia subtypes are related to gastric carcinogenesis. The detection rate of colorectal type chemosis was correlated with the number of biopsy blocks. Although the value of predicting the risk of gastric cancer based on the subtypes of enterocytosis is still controversial, it is clear that the more extensive the range of enterocytosis, the higher the risk of gastric cancer. What is pre-cancerous gastric lesion? In the pathological examination of chronic gastritis, the terms precancerous disease and precancerous lesion often appear. Precancerous disease refers to clinical disease, such as precancerous disease of gastric cancer as atrophic gastritis, gastric polyp, gastric ulcer, remnant stomach, etc. Precancerous lesions refer to pathological histological lesions, such as heterogeneous hyperplasia. Heterogeneous hyperplasia is also called intraepithelial neoplasia (a term recommended by the International Agency for Research on Cancer) Heterogeneous hyperplasia is divided into two grades: mild and severe (low grade and high grade). Mild heterogeneous hyperplasia can be caused by inflammation and must be observed regularly For severe heterogeneous hyperplasia, the annual cancer rate of atrophic gastritis is about one, and these patients need to be followed up regularly to improve the diagnosis rate of early gastric cancer.