After years of analysis and research by the World Health Organization and the National Institutes of Health, Helicobacter pylori (HP) was recently officially listed as the primary carcinogenic factor for gastric cancer. Researchers have proven through numerous epidemiological surveys that H. pylori has a close correlation with gastric cancer, and there have also been numerous laboratory studies in recent years that have confirmed that H. pylori infection can activate proto-oncogenes, inactivate oncogenes, and present abnormal expression of oncogenes. Researchers have found that H. pylori can produce a variety of pathogenic factors, including urease, an enzyme produced by H. pylori that hydrolyzes urea and releases ammonia, a “toxin” that can cause direct damage to the gastric mucosa. The toxins of H. pylori and other pathogenic factors of H. pylori, such as lipopolysaccharide, protease and phospholipids, work together to produce a local inflammatory and immune response to the gastric mucosa, and the damaged gastric mucosa is more vulnerable to gastric acid and pepsin, which eventually destroys the gastric mucosal barrier. Long-term chronic inflammation can stimulate cell proliferation, which not only increases the chance of spontaneous DNA replication errors, but also increases the likelihood of DNA damage by foreign mutagenic factors. Researchers have concluded that H. pylori acts as an initiating factor in gastric carcinogenesis, acting together with other factors to promote the transformation of normal gastric mucosal cells to gastric cancer.