Diabetes mellitus is not just one disease, but a progressive, multifactorial, heterogeneous group of disorders clinically characterized by obesity, insulin resistance and pancreas β-cell dysfunction. Current estimates demonstrate that diabetes affects 23.6 million people in the United States alone, which represents 7.8% of the population, and close to 250 million people worldwide [1]. Twin studies suggest a modulating role for genetic factors in the susceptibility to type 2 diabetes mellitus (T2DM) [2]. Pharmacologically, an extensive range of oral anti-diabetic drugs for type 2 diabetes exist for the treatment of T2DM, including insulin and its analogues, sulfonylureas, biguanides, thiazolidinediones (TZDs), meglitinides, α-glucosidase inhibitors. Although a variety of pharmacological treatments available, response, doses and tolerability to drugs are highly variable with many patients initially respond to anti-hyperglycemic drugs, yet over time, failing to react to mono-therapy. By far, a large inter-individual variability in drug response has been noticed and a number of factors validated to contribute to those differences in drug response including age, sex, disease, drug and food interactions, comorbidity, as well as genetic factors. Genetic variability in genes coding for drug-metabolizing enzymes, drug receptors and proteins involved in pathway signaling is a vital factor determining inter-individual variability in drug response [3].

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