This model of type 1 diabetes holds advantages over other models for the study of diabetic cardiomyopathy, in that the direct toxic effects associated with streptozotocin administration on tissues including the heart2,25–27 are avoided, along with the confounding effects of obesity and/or altered leptin signalling seen in models such as the ZDF rat. The gene discussed is LEP; the disease is diabetic cardiomyopathy.