This was seen in association with increased baseline and post-prandial intact GLP-1 concentrations, reduced post-prandial glucagon levels and sustained insulin levels, which in the presence of lower glucose levels resulted in an increase of insulinogenic index as a sign of stimulated beta-cell function, which provided a first insight into the mechanism of action of DPP-4 inhibition in type 2 diabetes (Figure 4). The gene discussed is GLP1R; the disease is type 2 diabetes mellitus.