Due to the β-cell-intrinsic role of TALK-1 L114P channels, the effect of somatostatin on glucose-stimulated insulin secretion might be limited; however, it remains to be determined if the fasting hyperglycemia observed in KCNK16-MODY patients is due in part to elevated glucagon secretion. This evidence concerns the gene KCNK16 and Hyperglycemia.