Through the activation of antioxidant response elements (AREs) and regulation of phase II detoxification enzymes, Nrf2 ensures the maintenance of redox homeostasis and supports cytoprotective functions under pathological conditions.[3] Notably, preclinical studies have demonstrated that Nrf2 activation attenuates key drivers of sepsis-induced organ dysfunction, including hyperinflammatory responses[4] and oxidative damage.[5] These effects are particularly evident in mitigating complications such as acute lung injury, acute kidney injury, and sepsis-associated myocardial depression. Here, NFE2L2 is linked to kidney injury.