Although speculative, reversal of the NCX function mode by the influx of Na+ represents an alternative mechanism for dysrhythmias (including bradycardia) in some inherited cardiac sodium channelopathies, such as the type 3 long QT syndrome associated with SCN5A mutations and persistent sodium currents (Remme and Bezzina, 2010). The gene discussed is SCN5A; the disease is Bradycardia.