Many studies have linked changes in mitochondrial oxidative phosphorylation to the development of insulin resistance and diabetes [14], [16], [25]: Importantly, a recent study in tissue specific muscle- and liver AIF knockout mice and Hq mice with a global AIF deficiency shows that a primary OxPhos defect alone does not cause diabetes, but rather increases insulin sensitivity and reduces fat mass [15]. The gene discussed is INS; the disease is diabetes mellitus.