In addition to its primary role in pro-inflammatory properties, IL-17 also contributes to the maintenance of gut homeostasis by serving multiple functions, including the regulation of Paneth cells.9–11 The lack of IL-17 signaling has been shown to cause Paneth cell deficiency, as observed in mice deficient in IL-17 receptor53 or RORγt,54 but it was unclear how IL-17 signaling regulates Paneth cells. This evidence concerns the gene IL17A and hyperinsulinemic hypoglycemia, familial, 4.