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For patients with HNF1A - MODY, HNF4A - MODY, and ABCC8 - MODY, SUs stimulate insulin secretion by enhancing ATP-independent closure of the K ATP channels, and therefore, bypass the low level of ATP in the pancreatic cells or decreased sensitivity to ATP.37 Although the transcription factor Hnf1b has a very similar structure to the transcription factor Hnf1a and shares a DNA-binding site, mutations in HNF1B result in reduced cell function due to pancreatic hypoplasia and increased hepatic insulin resistance