Previous studies have determined that SCN5A mutations can induce a decrease in the amount and function of Nav1.5, using genetic, electrophysiological, and molecular methods, leading to a series of VA such as LQT3, BrS, torsades de pointes, and idiopathic ventricular fibrillation. This evidence concerns the gene SCN5A and paroxysmal familial ventricular fibrillation.