In cisplatin-induced AKI model, cisplatin-induced mitochondrial damage and mtDNA leakage into the cytosol in renal tubular cells, and damaged mtDNA subsequently increased the activation of cyclic guanosine monophosphate–adenosine monophosphate (GMP–AMP) synthase (cGAS)-stimulator of interferon genes (STING) pathway, resulting in the activation of UPR response and then renal inflammation and AKI progression [84]. This evidence concerns the gene CGAS and acute kidney injury.