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The occurrence of gastric cancer is a multi-step and multi-factor progressive process. Under normal conditions, the proliferation and apoptosis of gastric mucosal epithelial cells maintain a dynamic balance. The maintenance of this balance depends on the joint regulation of oncogenes, oncosuppressor genes and some growth factors. In addition, cyclooxygenase-2 (COX-2) also plays an important role in the development of gastric cancer.<br />The oncogenes related to the development of gastric cancer include ras gene, bcl-2; The tumor suppressor genes included wild-type P53, APC, DCC, MCC, etc. Growth factors include epidermal growth factor (EGF), transforming growth factor-α (TGF-α), etc. Once this balance is disrupted, namely, oncogenes are activated, oncosuppressor genes are inhibited, growth factors are involved and DNA microsatellites are unstable, which causes excessive proliferation of gastric epithelial cells and fails to initiate apoptosis signals, and may gradually progress to gastric cancer. A variety of factors can affect the above regulatory system and participate in the occurrence of gastric cancer.