The β-cellis a major target organ in the pathogenesis of type II diabetes as evidenced bythe fact that overt diabetes does not occur until β-celldysfunction/loss has proceeded to the point where hypersecretion of insulin canno longer compensate for peripheral insulin resistance [1].The predominant model of the molecular events leading to β-cellfailure is that the diabetic environment, in particular chronically high levelsof glucose and free fatty acids, has toxic effects on the β-cell[2]. The gene discussed is INS; the disease is type 2 diabetes mellitus.