Although the vast majority of long-QT3 and Brugada syndrome mutations may not directly alter Nav1.5 palmitoylation, increased palmitoylation of Nav1.5 is predicted to enhance EADs and arrhythmias in patients with long-QT3 and reduced palmitoylation of Nav1.5 is expected to exacerbate symptoms in patients with Brugada syndrome; thus regulation of Nav1.5 activity by palmitoylation could be important in multiple cardiac pathophysiological conditions. This evidence concerns the gene SCN5A and cardiac arrhythmia.