Extensive preclinical and clinical evidence supports the renoprotective role of NRF2: animal studies have shown that NRF2 deficiency exacerbates injury in models of ischemia–reperfusion injury (IRI), unilateral ureteral obstruction (UUO), and hyperuricemic nephropathy, while its activation alleviates oxidative stress, inflammation, and fibrosis [18,19,20,21,22,23]. This evidence concerns the gene NFE2L2 and kidney disorder.