Voltage-gated sodium channels, specifically NaV1.5 located in the cardiac myocytes, are key drug targets in treating various diseases of the cardiovascular system, including heart failure, angina, and arrhythmia.1 The most common and lethal forms of arrhythmia result from a mutation in the SCN5A gene, which encodes the NaV1.5 channel subunits. This evidence concerns the gene SCN5A and cardiac arrhythmia.