Gastroenteropancreatic neuroendocrine tumors are a relatively rare but increasing group of tumors. Among them, neuroendocrine tumors occurring in the stomach have different characteristics from other sites and are described as bizarre. Gastroenteropancreatic neuroendocrine tumors can be pathologically classified into 3 grades according to the degree of tumor cell proliferation, namely G1, G2 and G3, while gastric neuroendocrine tumors, in addition to G1, G2 and G3 grades, are also classified into 4 types according to the degree of pathological differentiation and pathogenesis, namely well-differentiated type I, type II and type III gastric neuroendocrine tumors and poorly differentiated gastric neuroendocrine carcinoma (or type IV). endocrine carcinoma (or type IV). These four types of gastric neuroendocrine tumors have their own characteristics in terms of pathogenesis, clinical manifestations, diagnosis, treatment and prognosis. The normal gastric mucosa contains three major types of neuroendocrine cells that regulate gastric acid secretion, including G cells, ECL cells and D cells. Among them, G cells can secrete gastrin, which stimulates gastric acid secretion; ECL cells can secrete histamine, which also stimulates gastric acid secretion; and D cells secrete growth inhibitory hormone, which inhibits gastric acid secretion. Type I gastric neuroendocrine tumor is the most common type of gastric neuroendocrine tumor, accounting for about 70~80% of the cases. The pathogenesis of gastric neuroendocrine tumor is as follows: the lack of gastric acid based on chronic atrophic gastritis caused by various reasons, which feedback causes G cells in the gastric sinus to secrete excessive gastrin. Gastric neuroendocrine tumors. Type II gastric neuroendocrine tumors are rare and their development is also associated with high blood gastrin levels, but this elevated gastrin is derived from gastrinomas, another type of neuroendocrine tumor that occurs in the duodenum and pancreas, which can secrete excessive gastrin without any regulation, and this ectopic gastrin can, on the one hand, stimulate excessive secretion of gastric acid, causing hypertrophy of the stomach wall and even On the one hand, these ectopically produced gastrin stimulate excessive secretion of gastric acid, resulting in hypertrophy of the gastric wall and even multiple ulcers, and on the other hand, they can also promote the proliferation of gastric ECL cells. Gastric neuroendocrine tumors can be either disseminated or a component of multiple endocrine adenoma type 1 (referred to as MEN-1, an autosomal dominant disorder caused by mutations in the MEN-1 gene). Type III gastric neuroendocrine tumors have a different pathogenesis than types I and II and are not associated with hypergastrinemia or other gastric underlying disorders. Type IV gastric neuroendocrine tumors present pathologically as poorly differentiated neuroendocrine carcinomas, which are significantly different from both types I-III. Gastric neuroendocrine tumors of type I are often found incidentally by gastroscopy and present as polypoid lesions or submucosal masses, mostly less than 25 px in diameter, with a pathologic classification of G1, most often in the body or fundus of the stomach, often combined with atrophic gastritis, and with gastric acid deficiency and hypergastrinemia. Type II gastric neuroendocrine tumors are characterized by hypertrophy, edema, and even ulceration of the gastric mucosa, as well as multiple polypoid or submucosal lesions on top of this, with a pathological classification of G1 and G2. These patients have significantly elevated gastric acid and gastrin levels. If a type II gastric neuroendocrine tumor is found clinically, it is important to look further to find out where the gastrinoma causing the high gastrin levels is located (duodenum or pancreas), as well as to do pituitary, parathyroid and adrenal related hormone and imaging tests for the presence of MEN-1. Type III gastric neuroendocrine tumors differ from the previous two types in that type III does not have hypergastrinemia and the gastroscopic tumor is often Type III is a solitary tumor, often larger than 50 px in diameter, with polypoid or ulcerative lesions, and a pathologic grade of G1, G2, and some well differentiated G3. Type IV is a very poorly differentiated neuroendocrine carcinoma with a pathologic grade of G3, and the patient does not have hypergastrinemia. Skyrocketing differences in treatment and prognosis Type I gastric neuroendocrine tumors can be selected for gastroscopic resection, surgical sinusotomy or even total gastrectomy depending on the size and number of tumors and the depth of invasion. In terms of prognosis, type I gastric neuroendocrine tumors are biologically inert, with a metastasis rate between 2-5%, and have a better prognosis. The key to the treatment of type II gastric neuroendocrine tumors is to find the culprit gastrinoma and to remove it surgically. For gastric neuroendocrine tumors themselves, endoscopic or surgical resection can be chosen depending on the extent of the lesion. If no gastrinoma is found or if the gastric neuroendocrine tumor itself has metastasized, proton pump inhibitors and growth inhibitor analogs are used to control the symptoms of hyperacidity and inhibit tumor growth. Patients with combined MEN-1 will need to manage other sites of tumor such as pituitary, parathyroid, and adrenal glands as well. In terms of prognosis, type II gastric neuroendocrine tumors have a higher probability of metastasis than type I, which is about 10-30%. Type III gastric neuroendocrine tumors should be treated with aggressive surgery, including resection of the primary tumor and lymph node dissection. In terms of prognosis, type III gastric neuroendocrine tumors are more aggressive than the first two types, and invade the deep muscle layer of the gastric wall, and lymph node metastasis and liver metastasis are both common. Type IV gastric neuroendocrine tumors have poor pathological differentiation and very high malignancy, and most of them are in the progressive stage when detected. Treatment is based on surgery and chemotherapy.