Single nucleotide polymorphisms of the TCF7L2 gene demonstrate the strongest association with the risk of developing type 2 diabetes, linking its effects to changes in insulin secretion. The mechanism of action of hypoglycaemic drugs used in treatment of type 2 diabetes is, to a certain extent, related to their influence on the function of β-cells, which implies that variants of the TCF7L2 gene will affect the therapeutic effect of certain anti-hyperglycaemic drugs, including the variability in the effects of incretin-based therapy, and sulphonylurea derivatives. Along with the direct influence of the TCF7L2 gene on the function of β-cells, there is evidence of the effects of TCF7L2 gene polymorphism on the susceptibility to external risk factors associated with the development of type 2 diabetes, including the alimentary factors. Pharmacogenetic studies in diabetology have at present the greatest potential in terms of selection of the optimal comprehensive anti-hyperglycaemic therapy based on preliminary genetic testing, which might improve the outcomes of treatment and the prognosis for the course of type 2 diabetes, reducing the number of life-threatening complications. Key words: GPP-1 agonists, TCF7L2 gene, metformin, nutrition, type 2 diabetes, sulphonylureas