Herein, we discuss aspects of the recently reported study by Crippa et al, “Surgical Management of Insulinomas: Short- and Long-term Outcomes After Enucleations and Pancreatic Resections,”1 in terms of effective perioperative management of multiple endocrine neoplasia type 1 (MEN1)–associated insulinomas. Crippa et al concluded that surgical management of insulinomas can provide satisfactory outcomes with no mortality and good functional results.1 They also revealed that insulinomas associated with MEN1 have a higher risk than those not associated with MEN1 for being malignant and multifocal and that their curative treatment requires pancreatic resection.1 Multiple endocrine neoplasia type 1 is an autosomal dominantly inherited endocrine tumor syndrome characterized by tumor development in endocrine organs such as the parathyroid, endocrine pancreas, anterior pituitary, and adrenal cortex.2 A recent multicenter study in Japan reported that primary hyperparathyroidism, gastroenteropancreatic neuroendocrine tumors (GEP-NETs), and pituitary tumors were seen in 94.4%, 58.6%, and 49.6% of patients with MEN1, respectively.2 The presence of GEP-NETs, which includes insulinomas, is one of the most major prognostic factors for patients with MEN1, and surgical resection of these tumors is the most effective therapy to improve long-term prognosis.3 Despite these findings, the optimal perioperative management of patients with MEN1-associated insulinoma remains unclear. The article by Crippa et al1 contributes to our understanding of the efficacy of surgical management for MEN1-associated insulinomas; however, there are 3 points that are not fully addressed by this study.1 These points are: (1) It is not clear how the location of MEN1-associated multifocal insulinomas with malignant potential is identified to achieve curative surgical resection. (2) It is not clear how perioperative glycemic control is achieved in patients with insulinoma. (3) It is not clear if there are differences in tumor location between patients with and without MEN1.