A classical method of supporting disease causality in LQTS is electrophysiological examination of mutated channel proteins to disclose a reduction in repolarising K+- current (KCNQ1, KCNH2, KCNE1, KCNE2) or late persistence of depolarising Na+- current (SCN5A) [2]. This evidence concerns the gene SCN5A and familial long QT syndrome.