SCN10A and atrial fibrillation: Similar association studies have also identified a similar link between genetic variants in SCN10A and atrioventricular conduction properties as well as atrial fibrillation, adding further support for a significant role of Nav1.8 in cardiac electrophysiology.[57–59] Although the deletion or inhibition of Nav1.8 does not seem to adversely affect cardiac output in mice, the role of Nav1.8 in cardiac conduction will nevertheless be an important consideration when developing potential analgesics.[54,60]