Accumulating data suggest that severe glucotoxic blunting of an intracellular pathway leading to insulin secretion may contribute to the reversible beta cell dysfunction characteristic of KPDM patients.[20] One prospective study of patients presenting with DKA demonstrated a lower glucagon-mediated C-peptide response in obese patients with diabetic ketoacidosis compared with ketosis-resistant hyperglycemia patients, suggesting that there may be other causes and mechanisms involved. This evidence concerns the gene INS and Hyperglycemia.