It is interesting to speculate a three-way effect of metformin on mitochondrial function in diabetes-accelerated atherosclerosis, (1) by inhibiting redox shuttle enzyme mitochondrial glycerophosphate dehydrogenase and thus blocking glucose generation by gluconeogenesis, (2) by attenuating mitochondrial ROS generation by inhibiting mitochondrial complex I, and (3) by inhibition of DRP1-mediated mitochondrial fission (Madiraju et al., 2014; Hur and Lee, 2015). The gene discussed is DNM1L; the disease is diabetes mellitus.