Oxidative stress, characterized by an imbalance between prooxidants and antioxidants, plays a pivotal role in the pathogenesis and progression of hypertension through 2 primary mechanisms: direct damage by reactive species and dysregulated redox signaling.[17] Excessive oxidative stress is a pathogenic mediator of hypertension and a molecular trigger for CVD.[10] The renin–angiotensin–aldosterone system, particularly angiotensin II, activates NADPH oxidase (NOX), leading to superoxide production. The gene discussed is FMO5; the disease is hypertensive disorder.