Given the accumulating evidence demonstrating SOD2 as a specific target of SIRT3, and the pivotal role played by SIRT3 in promoting SOD2 activity through the regulation of SOD2 acetylation sites to maintain mitochondrial functions,[42, 43] it is worth noting that the mRNA expression of SIRT3 in AKI mice can be upregulated following treatment with irisin, MCM@MOF or MCM@MOF@irisin (data not shown). The gene discussed is SOD2; the disease is acute kidney injury.