Neuroendocrine tumors are a heterogeneous group of tumors originating from peptidergic neurons and neuroendocrine cells that can occur in many organs and tissues throughout the body, including the gastrointestinal tract, pancreas, bile ducts, liver, bronchi, lungs, thyroid, parathyroid, adrenal medulla, and paraganglia. It is a heterogeneous group of tumors showing a range of biological behaviors from inert and low malignancy to significantly malignant, highly aggressive and metastatic. In the last 30 years, the incidence and prevalence of NEN have increased significantly with the advancement and widespread use of diagnostic techniques such as endoscopy and biomarkers. Data show that the incidence of NEN has increased by as much as 500% over the past 30 years, with an incidence rate of 5.25/100,000, of which gastroenteropancreatic neuroendocrine tumors (GEP-NEN) account for 65%-75%. Neuroendocrine tumors (NEN) are classified as functional or non-functional. Functional NEN can produce endocrine hormones or peptides released into the blood, producing a range of clinical manifestations. Patients with non-functional NEN may have elevated hormone levels in blood and urine, but do not exhibit specific symptoms or syndromes, and when the tumor increases in size to a certain extent, symptoms related to tumor compression occur. The prognosis of patients with G1/G2 stage of neuroendocrine tumor is good. Even if the tumor metastasizes, the prognosis of these patients is very different from that of patients with cancer in the corresponding area, so these patients should be resected by R0 as much as possible, and R1 resection can also be considered. The purpose of surgical resection is to reduce the tumor, improve the symptoms and enhance the quality of life. The prognosis of stage C3 neuroendocrine tumor patients is poor, and the principles of surgery are similar to those of cancer. Anti-endocrine therapy: growth inhibitor analogs (SSA) are the standard treatment for functional neuroendocrine tumors at any site. Interferon alpha (IFN-α) can be used for symptom control in patients who are intolerant to SSA. Due to the toxicity of IFN, it is usually used as second-line therapy. Anti-proliferative therapy: For advanced neuroendocrine tumors, anti-proliferative agents include biological agents (SSA, IFN-α), molecularly targeted agents (sunitinib, everolimus) and chemotherapeutic agents (streptomycin, fluorouracil, adriamycin, temozolomide and capecitabine). The selection of the above drugs should be considered in the context of tumor load, rapidity of progression, drug toxicity and side effects, individualized patient status and the availability of surgery. Local treatment Gastroenteropancreatic neuroendocrine tumors are prone to liver metastasis, and hepatic artery (chemo) embolization is feasible for such patients, with an efficiency of more than 50%. PRRT can be a treatment option for patients with neuroendocrine tumors if growth inhibitor receptor imaging (SRS) indicates radioactive uptake of the lesion. Currently, the radioisotopes commonly used for clinical labeling are 90 yttrium (90Y) and 177 lutetium (177Lu), which differ in the type of radiation, particle energy and tissue penetration capacity. The partial remission rate for patients undergoing PRRT for GEP-NET is 10%-37%, and PRRT can be selected for second-line and beyond in patients who have failed drug therapy and are SRS-positive.