Therefore, glucokinase has a central role in glucose homoeostasis and the blood glucose threshold was set at 4 to 6.5 mmol/L.[1] The mutation of human GK gene causes the decrease of GK activity in β - cells and the increase of blood glucose threshold, which leads to moderate fasting hyperglycemia in Mody patients.[2] It has been confirmed clinically that impaired GK can cause glucose metabolic diseases including the most common T2DM.[3,4] GKA can effectively reduce glycosylated hemoglobin level and improve β-cell function in T2DM by improving GK function. Here, GK is linked to Hyperglycemia.