When, more than two decades ago, I started working as a physician providing medical care to patients with diabetes, I was completely unaware of the diversity of its forms. At that time, I knew only that there was an insulin-dependent diabetes (renamed later as type 1) and a non-insulindependent diabetes (currently known as type 2). I am convinced that this was the predominant viewpoint at that time. Over the last 20 years, however, scientists—both basic researchers and clinicians—have discovered and characterised more than 20 forms of monogenic diabetes [1– 3]. The term MODYattracted my attention in the early 1990s when discoveries of its molecular basis were emerging [4, 5] and my personal interest in the genetics of diabetes was growing. It should be noted that much earlier there were some bright physicians whose brilliant observations pointed to rare cases of patients with diabetes who have a very rich family history of this disease and whose symptoms did not fit into either of the two categories identified at that time [6, 7]. These patients shared some common features, such as an autosomal dominant inheritance and abnormalities of insulin secretion; they were also usually thin and noninsulin-dependent. We later learnt that MODY was not a uniform entity but, rather, constituted a heterogeneous group that included several forms of single gene diabetes [8, 9]. Clinically, patients with MODY exhibited different degrees of hyperglycaemia, rates of disease progression, responses to pharmacological treatment and concomitant extra-pancreatic features. Individuals involved in MODY research revealed the origin of these differences and learnt how to use them in medical practice [2, 10–12]. Although the molecular aetiology of MODY has not yet been fully dissected, genetic testing is now available for the most prevalent subtypes. To date, thousands of MODY patients have been diagnosed all over the world, most of them probably thanks to research projects. These individuals, along with their families, benefited from genetic testing. Many patients, mainly carriers of the HNF1A mutation, were able to switch from insulin to sulfonylurea [13, 14]. Not only did their glycaemic control improve [14], but it is likely this switch also enhanced their quality of life. Some other patients, mostly individuals with GCK mutations, were able to discontinue pharmacological treatment altogether and controlled their diabetes through diet alone [15]. The genetic diagnosis also defined the prognosis for the disease progression or, in predictive testing, the risk of diabetes development in the examined individuals and their relatives. One may assume, although this has yet to be M. T. Malecki (*) Department of Metabolic Diseases, Jagiellonian University Medical College, 15 Kopernika Street, 31-501 Krakow, Poland e-mail: malecki_malecki@yahoo.com