The most common causes are mutations in Glucokinase (GCK), presenting as mild non-progressive hyperglycemia since birth [4]; hepatocyte nuclear factor-1 homeobox A (HNF1A) and hepatocyte nuclear factor-4 homeobox A (HNF4A), presenting as familial symptomatic diabetes whereby hyperglycemia usually becomes evident during adolescence or early adulthood and deteriorates throughout life [5–7]; and hepatocyte nuclear factor-1 homeobox B (HNF1B), presenting mainly as renal alterations and diabetes [8]. This evidence concerns the gene HNF1A and diabetes mellitus.