In addition, loss-of-function mutations in the SCN5A gene encoding the pore-forming α-subunit of the cardiac sodium channel (Nav1.5) have been shown to underlie multiple inherited arrhythmia syndromes, including Brugada syndrome, cardiac conduction disease, sinus node dysfunction, sudden infant death syndrome, and atrial standstill, while SCN5A mutations resulting in a persistent or “late” sodium current have been associated with long-QT syndrome type 3 (for review, see Refs. This evidence concerns the gene SCN5A and atrial standstill.