STING-deficient mice showed improved inflammation and acute kidney injury (AKI) progression, evidenced by the deactivated mtDNA-cGAS-STING axis and the decreased phosphorylated TBK1 and p65.145 Aged microglia affirmed prominent cytosolic accumulation of mtDNA abundance and nucleoids adjacent to the mitochondria outer membrane, which triggered VDAC-dependent cGAS and several type I IFN and proinflammatory genes.146 To date, the mechanism of mtDNA release in these settings is not clear. This evidence concerns the gene VDAC1 and acute kidney injury.