Whereas the ROS-generating role of non-NADPH oxidases in cardiovascular cells seems to be minor in physiologic conditions,9 growing evidence suggests that ROS generated in mitochondria and the endoplasmic reticulum (ER) may contribute to oxidative stress in hypertension.10, 11, 12 This likely involves cross-talk between Noxs and mitochondria/ER. This evidence concerns the gene FMO5 and hypertensive disorder.