Self-DNA originates from dying cells and is readily oxidized under conditions of oxidative stress and inflammation.44 Oxidatively modification of self-DNA confers resistance to exonuclease TREX1-mediated degradation and potentiates STING-dependent immune sensing, thereby amplifying the inflammatory response.15,45 Furthermore, activation of the STING pathway in patients and mouse models has been associated with intensified tubular inflammation and AKI progression.37 However, our current study reveals that deletion of STING only moderately improves the survival of AKI mice. Here, STING1 is linked to acute kidney injury.