The activation of AT1R stimulates several downstream mediators, including AKT/ERK, TGF-β/Smad, MAP kinases, NADPH oxidase, NF-kB, and hypoxia inducible factor-1alpha (HIF-1α), which are involved in vasoconstriction, fibrosis, inflammation, oxidative stress, and ion channel abnormalities [1, 5–7], Ang II-mediated inflammation and oxidative stress are thought to promote atrial fibrosis in AF [2, 8, 9]. This evidence concerns the gene TGFB1 and atrial fibrillation.