For instance, mutations in the SCN5A gene that encodes the alpha-subunit of the sodium current (Nav1.5) have been found in 9% of an unselected AF population and in 6% of patients with lone AF.[1] Mutations of the SCN1B –SCN4B genes that encode the modifying beta-subunits of the Navß1-ß4 have been detected in an additional 2%.[2, 3] Other genes play an important role for the generation of a healthy Nav1.5 current by coding for accessory channel anchoring or trafficking proteins. This evidence concerns the gene SCN5A and atrial fibrillation.