Alternatively, diminished action of insulin and the resultant hyperglycemia may result in the accumulation of advanced glycation end-products (AGE) and this would increase oxidative/inflammatory events [237–239], which in turn would further increase the production of AGE, and thus creating a vicious cycle that potentiates the oxidative destruction of beta-cells in both T1D and T2D [237, 240–242]. This evidence concerns the gene INS and type 1 diabetes mellitus.