In an experimental setting in which a hERG activator was used to approximate SQT1, quinidine (a blocker of INa and IKr) was effective at extending atrial AP duration and ERP and preventing AF (Nof et al., 2010), more so than E-4031 (a selective IKr blocker) or lidocaine (an INa blocker) alone, suggesting that K+ and Na+ channel blocking effects combine synergistically for improved management of AF in SQT1. The gene discussed is KCNH2; the disease is atrial fibrillation.