SULT1A1 and acute kidney injury: 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.