As reviewed by Wilde and co-workers, DCM may be: (i) secondary to SCN5A mutation induced arrhythmias and/or bradycardia; (ii) due to increased late INa and consequent changes in intracellular Na+ and Ca2+; or (iii) secondary to the non-electrical role of NaV1.5 as a potential anchoring protein for structural and cytoskeletal proteins (33). This evidence concerns the gene SCN5A and cardiac arrhythmia.