Helicobacter pylori (HP) is a bacterium that is transmitted through the digestive tract mainly by damaging the gastric mucosa. It is not only the causative agent of gastritis and peptic ulcer, but is also currently included by the World Health Organization as a type I carcinogen (i.e., an identified human carcinogen), the most common causative agent of gastric cancer, the initiator of the evolutionary pattern of gastric cancer, and plays an important role in the process of gastric cancer development. Although HP infection is an important factor in causing gastric cancer, not all HP-infected patients will develop gastric cancer. In fact, the rate of H. pylori infection in the population is very high, and the rate of H. pylori infection in China is over 50%. Most of the infected people do not have stomach symptoms and may not develop gastric cancer in their lifetime. Statistics show that about 80% of Hp-infected patients have asymptomatic gastritis, 15-20% have peptic ulcers, 5-10% have Hp-related dyspepsia, and about 1% have gastric malignancies [gastric cancer, mucosa-associated lymphoid tissue (MALT) lymphoma], and most infected patients have no symptoms or complications, but the distribution of Hp-induced gastritis and gastric ulcers, gastric atrophy, and intestinal metaplasia and their severity are closely related. The risk of gastric cancer is significantly increased in gastric body-dominated atrophic gastritis, especially when the degree is severe, while the risk of duodenal ulceration is increased in patients with sinus-dominated gastritis. Under what circumstances do we need to screen and treat for H. pylori? What is the significance of treatment? Screening and treatment of Hp in patients with definite peptic ulcers promotes peptic ulcer healing and significantly reduces the rate of ulcer recurrence and complications; Hp gastritis with dyspeptic symptoms is preferred in patients with Hp gastritis, and eradication of Hp results in long-term symptom relief in some patients; eradication of Hp is the first-line treatment for localized stage (Lugano I/II) gastric MALT lymphoma; long-term administration of PPI alters the distribution of Hp gastritis and increases the risk of gastric body gastritis, and eradication of Hp reduces this risk; there is evidence that Hp infection is associated with unexplained iron deficiency anemia, idiopathic thrombocytopenic purpura, vitamin B12 deficiency, and other disorders. In these diseases, Hp should be detected and eradicated; Hp gastritis can increase or decrease gastric acid secretion, and eradication therapy can reverse or partially reverse these effects Hp; Hp eradication significantly improves the inflammatory response of the gastric mucosa, stops or delays the onset and progression of gastric mucosal atrophy, intestinal chemosis, and partially reverses atrophy, but makes it difficult to reverse intestinal chemosis; individuals at high risk of gastric cancer [family history of gastric cancer, early gastric cancer endoscopic The optimal cut-off age for treatment of Hp infection to prevent gastric cancer remains unclear; it is indicated in the older age group, while screening for Hp infection in childhood is not recommended to prevent gastric cancer. Although Hp eradication can be used as a primary prevention strategy, gastric cancer may still occur after successful eradication therapy. Hp eradication induces regression of gastric precancerous lesions, significant improvement in gastric mucosal inflammatory response, and improvement in gastric mucosal atrophy in some patients, but up to 45% of treated patients still show disease progression. Therefore, even if Hp is eradicated, regular follow-up and necessary screening and gastroscopy for high-risk groups are still necessary