Most studies in cell lines and animal models have considered that oxidative stress generated by reactive oxygen species (ROS) overproduction and inflammation mediate the CDDP-induced kidney damage; hence its inhibition may attenuate CDDP-induced nephrotoxicity.4–7 CDDP stimulates several antioxidant enzymes transcription via nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway deactivation, and induces intracellular injury through chemokines and other pro-inflammatory cytokines release via NF-κB activation.8,9. Here, NFE2L2 is linked to Nephropathy.