To further validate the role of STING pathway in AKI, we used Sting-knockout mice (Sting−/−) and stimulated them with cisplatin and AA I. As a result, Sting−/− mice exhibited lower elevated secretion of CXCL10 and IFN-β (Fig. 2f, g), and showed improved survival and decreased serum creatinine compared to wild-type (WT) mice, despite treatment with AA I and cisplatin (Fig. 2h–k). This evidence concerns the gene STING1 and acute kidney injury.