The most frequently observed forms of congenital LQTS arise from mutations to KCNQ1 and hERG (alternative nomenclature KCNH2), which respectively contribute to the slow delayed rectifier potassium current (IKs, LQT1) and the rapid delayed rectifier potassium current (IKr, LQT2); these account for 44% and 35% of cases, respectively [9]. Here, KCNH2 is linked to familial long QT syndrome.