Summary: By its very nature, type 2 diabetes is a progressive disease, largely due to the gradual loss of the ability of the pancreatic beta cells to secrete insulin. Therefore, although insulin resistance, the effects of which we can partially neutralise with metformin, is the primary cause of the onset of hyperglycaemia in patients with type 2 diabetes, sooner or later they will require the inclusion of a drug that increases insulin secretion, and some of them will require insulin treatment. Early intensification of type 2 diabetes therapy to achieve optimal glycaemic control is essential for the prevention of chronic complications associated with the disease, resulting in a longer and better quality of life for patients. It is important not to wait until glycaemia is significantly above target, as each month of poor diabetes control increases the risk of complications, and treatment with two or more drugs with different mechanisms of action increases the likelihood of achieving sustained normoglycaemia. Drugs to consider when intensifying diabetes treatment in a patient on metformin monotherapy are gliptins, which are inhibitors of dipeptidyl peptidase 4 (DPP4), an enzyme that breaks down the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). GLP-1 and GIP are secreted in the gastrointestinal tract after a meal and stimulate insulin secretion from pancreatic beta cells. Unfortunately, their duration of action is short as they are degraded within 1–2 minutes by DPP4, whose activity is increased in patients with type 2 diabetes. The prolongation of the half-life of GLP-1 and GIP by gliptins results in an increase in endogenous insulin secretion and a reduction in glycaemia. Combination therapy with gliptins and metformin is an effective and accessible treatment for type 2 diabetes with minimal risk of hypoglycaemia, and its use early in the course of the disease allows long-term normoglycaemia.