Therefore, even without any modifications in the voltage dependence and biophysical properties of NaV1.5, the absence of IK1 rectification and reduced pore conductance caused by the Kir2.1E299V mutation in atrial cardiomyocytes would be sufficient to underlie the initiation and maintenance of AF in the heterogeneous atria of a SQTS3 patient. This evidence concerns the gene SCN5A and atrial fibrillation.