Consistent with a critical role of mitochondrial dynamics in the progression of DKD, we have previously shown that kidney podocytes undergo a shift towards fragmented mitochondria and enhanced mitochondrial fission through a signaling cascade that involves dynamin related protein-1 (Drp1) phosphorylation at serine 600 residue and recruitment of Drp1 to the mitochondria that ultimately leads to increased production of mitochondrial ROS (mROS) and the progression of DKD13,14. This evidence concerns the gene DNM1L and diabetic kidney disease.