The purpose of this study is to test the following two hypotheses; 1) oxidative stress-mediated activation of CaMKII signaling with hydrogen peroxide (H2O2) in structurally remodeled atria characterized with increased atrial tissue fibrosis promotes AF by the mechanism of EAD and DAD-mediated triggered activity; and 2) selective inhibition of the enzymatic activity of CaMKII or its distal target, the INa-L with the specific INa-L blocker, GS-967, [18] suppresses the oxidative AF. The gene discussed is CAMK2G; the disease is atrial fibrillation.