Within the cardiovascular domain well-studied examples are HCM with three founder mutations being responsible for an estimated 40% of Dutch HCM patients [4, 11], the 1795insD mutation in the cardiac sodium channel (SCN5A) associated with a SCN5A-overlap syndrome (i.e., a disease entity with both gain of function (LQTS) and loss of function characteristics (progressive cardiac conduction disease and Brugada syndrome)) [7], a haplotype on chromosome 7 associated with idiopathic ventricular fibrillation [6], and the PLN Argdel14 mutation [8]. Here, SCN5A is linked to paroxysmal familial ventricular fibrillation.