These molecular events induce protein oxidation and dysregulated cell signalling, leading to inflammation, proliferation, apoptosis, migration, and fibrosis, which are important processes contributing to impaired vascular function, cardiovascular remodelling, renal dysfunction, immune cell activation, and sympathetic nervous system excitation in hypertension.1, 2, 3, 4 A major source of cardiovascular ROS is a family of nonphagocytic NADPH oxidases (Nox1, Nox2, and Nox4 in rodents and Nox1, Nox2, Nox4, and Nox5 in humans).5 This evidence concerns the gene NOX1 and hypertensive disorder.