The overall goal of our research unit is to understand metabolic control of insulin secretion and why it fails in type 2 diabetes (T2D). In recent years, this has meant that we have used information from GWAS (Genome-wide association study) to direct our efforts towards the genes which are actually linked to the development of the disease. To reach this overarching goal, we have worked along two lines: 1) mitochondrial (dys)function in ß-cells and, 2) melatonin signaling in islets. In fact, these projects have emanated from findings in GWAS, where genetic variants of Transcription factor B1 mitochondrial (TFB1M) and the Melatonin receptor 1B have been robustly associated with T2D. Overall, our work holds promise to increase understanding of how T2D evolves. Mitochondrial function is difficult to target with drugs. In contrast, the melatonin receptor 1B is a potential drug target in T2D.