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). This evidence concerns the gene TLX2 and Bradycardia.