There are numerous hypotheses explaining the association of different aspects of abnormal mitochondrial function to diabetes—from decreased mitochondrial content and disturbances in mitochondrial biogenesis [7], to impaired mitochondrial function leading to intracellular accumulation of lipid products and increased production of reactive oxygen species (ROS) [8], that all further impair insulin sensitivity and energy metabolism (reviewed in detail by Patti and Corvera) [9]. The gene discussed is INS; the disease is diabetes mellitus.