In streptozotocin (STZ) induced diabetic mice models, STZ injection led to β cell destruction in all the animals, in which p16INK4a-/- mice showed much lower blood glucose levels in comparison with the persistent hyperglycemia in p16INK4a+/+ and p16INK4a+/- groups, suggesting that the β cells in p16INK4a-/- mice probably have better regeneration capacity after STZ damage. This evidence concerns the gene CDKN2A and Hyperglycemia.