Temple et al. [30], demonstrated that: K+ currents (total currents and those sensitive to the IKCNQ1/IKs blocker chromanol 293B) were significantly higher in atrial cells from the mice with deletion of the KCNE1 gene than in controls, and when CHO cells were driven at very rapid rates (comparable to the normal mouse heart and to human AF), the sigmoidicity displayed by the activating IKs results in much less current accumulation compared with IKCNQ1 alone. This evidence concerns the gene KCNE1 and atrial fibrillation.