The rationale for flecainide use for treatment of CPVT is supported by in vitro studies demonstrating that flecainide blocks RyR2 in lipid bilayers (27) suppresses calcium waves in CASQ2-knockout myocytes, abolishes delayed afterdepolarization–mediated triggered activity, and reduces exercise induced ventricular arrhythmias inCASQ2 and RYR2 mouse models. The gene discussed is CASQ2; the disease is Ventricular arrhythmia.