Mutations in KCNQ1, hERG and SCN5A can cause LQTS through either a loss-of-function of potassium channels (IKs and IKr) or a gain-of-function of sodium channel leading to an increase in the late INa, lengthening the cardiac APD and manifesting as a prolonged QT interval7. This evidence concerns the gene KCNQ1 and familial long QT syndrome.