Recent publications further confirmed that GCK may be associated with non-insulin-dependent diabetes mellitus [73,74], maturity-onset diabetes of the young, type 2 [74], and persistent hyperinsulinemic hypoglycemia of infancy [75], thereby validating the potential biological contributions of obesity to this endocrine pathogenesis. This evidence concerns the gene GCK and obesity due to melanocortin 4 receptor deficiency.