We hypothesise that increased K<sub>ATP</sub> channel activity and/or intra-islet somatostatin may contribute to the glucagon secretion defects seen in T1D and that these issues can be addressed with sulfonylureas or SGLT2 inhibitors.<h4>Methods</h4>We first tested this hypothesis in vitro by comparing glucagon secretion in response to increasing concentrations of the sulfonylurea tolbutamide-used to titrate K<sub>ATP</sub> channel activity-in isolated human islets from donors with T1D and healthy donors without a history of diabetes. This evidence concerns the gene SLC5A2 and diabetes mellitus.