The human atrium chiefly expresses Cx40 and Cx43, and abnormalities in Cx40 levels and distribution were prevalent in AF.44 Previous pre-clinical work has also shown that Cx40-KO increases the susceptibility to atrial arrhythmias in mice.45 Similarly, Cx43 plays a crucial role in cardiac development and down-regulation of Cx43 triggers sympathetic AF.46 These studies all highlight the contribution of the abundance and distribution of gap junctions to the maintenance of normal electrophysiology. The gene discussed is GJA1; the disease is atrial fibrillation.