To this end, we argued that forced expression of the NDUFS4 subunit, consistently downregulated in the podocytes of the type 1 and type 2 diabetic mice as well as in the glomeruli of the DKD patients, might overcome the mitochondrial maladaptation in DKD and provide significant insights into molecular mechanisms of its progression. The gene discussed is NDUFS4; the disease is diabetic kidney disease.