Whilst it is important that both assumptions and potential limitations of the models used in this study are made explicit, these do not influence fundamentally the conclusions that can be drawn on likely mechanisms by which the KCNQ1 V307L mutation facilitates arrhythmia induction and maintenance, and the possibility of IKs inhibition as pharmacological modulation in the setting of SQT2. Here, KCNQ1 is linked to cardiac arrhythmia.