Recent studies have indicated that somatostatin and its analogs have obvious anti-proliferative effects on various solid tumors, such as gastroenteropancreatic neuroendocrine tumors and breast cancer, which are mediated through somatostatin receptors [1,2], but some clinical research have indicated that the impact of somatostatin and its analog receptor expression levels on outcomes in patients with pancreatic neuroendocrine tumors (PNETs) has not been evaluated [3,4]. This evidence concerns the gene SST and pancreatic neuroendocrine tumor.