The current study using Sult1a1-deficient (Sult1a1-/- KO) mice provides the first evidence that SULT1A1 contributes as a key modulator in the progression of cisplatin-induced AKI by producing IS that evokes reactive oxygen species (ROS) through an aryl hydrocarbon receptor (AhR) and downregulation of antioxidant enzymes in the kidney. This evidence concerns the gene AHR and acute kidney injury.