NOX2 is also a critical mediator of AF pathophysiology through its modulation of acetylcholine-activated inward-rectifying potassium current (IKACh) via protein kinase C-ε (PKC-ε) translocation to the cell membrane, and NOX2 knockdown reduces the onset of AF in canines (17–19). This evidence concerns the gene CYBB and atrial fibrillation.