For peptic ulcer disease, the etiological role of H. pylori infection has been proven, 60-90% of gastric cancer cases are associated with H. pylori. The bacterium is recognized as a first-order carcinogen. An association has been established between the successful elimination of H. pylori and a reduced risk of gastric cancer and relapse of peptic ulcer. In the pathogenesis of chronic inflammation in the gastric mucosa associated with H. pylori, there are reference points that determine the further path of development of the pathology. If peptic ulcer is not a consequence of the direct damaging effect of NSAIDs, it is associated with the development of gastritis. In gastric ulcer, gastritis is found in both the antrum and the fundus of the stomach Atrophy of the glands begins in the antrum, then its foci are found in the fundus on the front and back walls. Gradu- ally they increase in size, merge with each other, the acid secreting zone decreases, and the border between the fundus and pyloric glands shifts in the proximal direction. With atrophic fundus gastritis, the likelihood of developing high ulcers and stomach cancer increases. Significant increase in apoptosis processes with relative rigidity of proliferation leads to the formation of ulcer, and carcinogenesis is due to excessive proliferation and accumulation of cell mutations. One of the subjects of damage is Cag A H. pylori protein, which implements remodeling of the gastric epithelial barrier. Among its effects are modulation and impaired proliferation of gastric epithelium, leading to morphological changes. The aggressive action of Cag A protein enhances toxic doses of alcohol and smoking, supporting inflammation and causing damage to the gastric mucosa. Despite the common etiology and pathogenesis of gastric ulcer and gastric cancer, the relationship with the de- velopment of atrophic pangastritis and the similarity of convention risk factors determines that the key point in the manifestation of gastric cancer is a genetic predisposition in the form of gene polymorphism causing severe atrophy as a result of chronic inflammation.