However, we are aware that since the TCF7L2 variants increase progression from IGT to diabetes [5], additional models considering diabetes therapy, particularly including a control group having been treated with a different antidiabetic agent - e.g., metformin, would be desirable to clarify whether the observed data reflect pharmacogenetic effects specific to SUs or rather a disease-genetic process. Here, TCF7L2 is linked to diabetes mellitus.