Because the activation of the AT1 receptor stimulates NADPH oxidase activity [153, 154] and because AT1 receptor increases with age and in response to 6-OHDA treatment [155], the authors propose that angiotensin II/AT1/Nox4 axis-mediated oxidative stress could contribute to damages in neurons in PD [90]. The gene discussed is FMO5; the disease is Parkinson disease.