CACNA1C and familial long QT syndrome: Gain-of-function mutations in the voltage-gated sodium channel (Nav1.5) [8] and the voltage-gated L-type Ca2+ channel (Cav1.2) [9,10,11,12] are strongly linked to LQTS, causing impaired channel inactivation, enhanced depolarisation and elevated calcium (Ca2+) influx, which prolongs the ventricular AP plateau [11].