Indeed, extensive evidence from several studies shows that genetic or pharmacologic activation of the Nrf2 antioxidant response leads to improved kidney injury outcomes in ischemia-reperfusion injury (IRI) [28] and aristolochic-acid-induced [29] AKI models in mice, and conversely, suppression of Nrf2 activity by chronic administration of N-acetyl-cysteine (NAC), an antioxidant, contributes to AKI to CKD progression [30]. Here, NFE2L2 is linked to chronic kidney disease.