The pathogenesis of this syndrome is unclear, even though the environmental factors, such as diet and physical activity, coupled with still largely unknown genetics factors clearly interact to produce the syndrome.[19] What causes the initial beta-cell insult leading to acute insulin deficiency? Glucose toxicity has been suggested as a contributing factor. 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. Prior studies by our group and other investigators indicate that most patients with ketosis-prone type 2 diabetes had a higher prevalence of a parental history of diabetes and were generally more obese.[13,15] Because of its association with obesity and hyperlipidemia as well as hyperglycemia, some investigators have examined whether high levels of free fatty acids or other lipids might be the trigger of unproved diabetic ketosis.[20] Is it possible that the ketosis-prone diabetes in Chinese patients represents an attack by disease sources factor such virus or bacteria? However, there is no evidence that those patients had an infectious illness.[7] Why are Asian more susceptible to glucose toxicity and lipotoxicity? Differences in the lifestyle, including the consumption of rice and wheat as staple food or gene-environment interactions may also have an impact on the incidence of KPDM and the findings call for further studies.[21]