Historically, much attention has been paid to PCK1 in the context of gluconeogenesis because 1) PCK1 is more abundant than PCK2 in the liver of rodents 3 (note: human PCK2 accounts for approximately 50%), 2) PCK1 expression and activity are dynamically regulated by nutritional and hormonal cues, including fasting 3, 3) overexpression of PCK1 in the liver caused hyperglycemia 17,18, and 4) inhibition of PCK1 attenuated hepatic gluconeogenesis from lactate/pyruvate, although liver-specific Pck1 knockout mice maintain euglycemia due to compensatory renal gluconeogenesis 19–24. This evidence concerns the gene PCK2 and Hyperglycemia.