SCN5A and heart conduction disease: Inversely, it remains to be tested whether mutations in intronic regions regulating alternative splicing of SCN5A exon 6A/6B might be considered as a cause of cardiac-conduction abnormalities in patients in whom no mutations were identified in the coding sequence of SCN5A. Also, if dysfunction of the cardiac sodium channel in DM is comparable in some aspects to cardiac-conduction disease caused by mutations in SCN5A, an attractive supposition would be that therapeutic approaches developed for these diseases could be considered for DM.