Given that angiotensin II or a high salt diet can induce NADPH oxidase activity and mitochondrial ROS production (Gill & Wilcox, 2006; Sachse & Wolf, 2007), and that increased GSH is known to suppress ROS, it is plausible that the observed increase in GSH will contribute to the inhibition of CKD progression. This evidence concerns the gene FMO5 and chronic kidney disease.