It was reported that oxidative stress affected the progression of diabetes mainly by the following two mechanisms [10]: (1) directly cause islet β-cell damage through disrupting mitochondrial structure, causing apoptosis, inhibiting energy metabolism, reducing insulin synthesis and secretion, affecting the normal function of islet β-cells, etc and (2) induction of insulin resistance through interfering with phosphorylation of insulin receptors and their substrates, affecting cell signaling pathways [31]. This evidence concerns the gene INS and diabetes mellitus.