To date, insulin resistance and impaired incretin action are thought to be central to the pathophysiology of pre-DM and T2DM [1], whereas some experts hypothesize and speculate that calcium homeostasis, inflammatory responses and oxidative stress, as well as vitamin D-regulated levels of adipokines, such as leptin and lipocalin, are some of the possible mechanisms of progression to T2DM [33,34], and the potential causes will require future further exploration. This evidence concerns the gene GCG and Insulin resistance.