The authors speculated that the C1019T variant might enhance the susceptibility to unstructured AF through two mechanisms: firstly, the variant affected the adhesion of monocytes to modulate the extent of local inflammation, which was increasingly recognized to be involved in the onset of AF; secondly, Cx37 was also expressed in vascular smooth muscle cells at the orifice of pulmonary veins and the variant altered the electrophysiological properties of gap junction channels, which might disturb cardiac conduction and contributed to AF. This evidence concerns the gene GJA4 and atrial fibrillation.