Loss-of-function gene variants in either gene reduce repolarizing force and delay ventricular repolarization, causing LQTS, particularly manifest (for KCNQ1 mutants) during periods of sympathetic stimulation such as while swimming (Wang et al., 1996; Tyson et al., 1997; Ackerman et al., 1999). This evidence concerns the gene KCNQ1 and familial long QT syndrome.