With respect to the implications of the effects of Testin on KCNE2 regulation of Kv1.5, we previously found that KCNE2 is required for normal Kv1.5 activity in ventricular myocytes; Kcne2 knockout in mice resulted in reduction in Kv1.5 current (and susceptibility to drug-induced LQTS) because without Kcne2, Kv1.5 trafficking to the intercalated discs was disrupted [34]. Here, KCNE2 is linked to familial long QT syndrome.