As proof-of-concept that SIRT3 has a role in the regulation of microtubule architecture, we took advantage of untreated SIRT3-deficient mice that, compared to their untreated wild-type (WT) littermates, showed a constitutive hyper-acetylation state of mitochondrial proteins (Supplementary Fig. 8A), an altered distribution and reduced expression of SOD2 and tubulin (Fig. 7i; Supplementary Fig. 8B), similar to that observed in mice with cisplatin-induced AKI showed in Fig. 7e. The gene discussed is SOD2; the disease is acute kidney injury.