In this context, sugar replacement is of interest, as (I) excessive sugar intake may contribute to obesity as an important risk factor for type 2 diabetes, (II) low-glycemic index diets may decrease the risk for type 2 diabetes development, (III) a lower intake of glycemic sugars could limit the high blood glucose people in people with impaired insulin sensitivity and (IV) a mechanistic basis exists by which high amounts of fructose impact hepatic de novo lipogenesis and the development of hepatic insulin resistance [9,10,11,12]. The gene discussed is INS; the disease is type 2 diabetes mellitus.