Similarly, patients with mutations in glucokinase, who suffer from maturity onset of diabetes in the young (MODY-2), appear to have normal incretin secretion (Murphy et al., 2009), suggesting that while the molecular machinery employed for glucose-sensing by the pancreatic β-cell is present, it does not seem to play as dominant a role in the stimulus-secretion coupling of either K- or L-cells. This evidence concerns the gene GCG and type 2 diabetes mellitus.