Attenuation of oxidative stress by the silencing of the NADPH oxidase 2 with a gene-based approach successfully prevented the electrical remodeling of atrial myocardium and maintenance of the arrhythmia in a canine model of AF [64], and gene therapy directed at the improvement of mitochondrial antioxidative capacity may also be effective in prevention of AF. Here, CYBB is linked to atrial fibrillation.