Due to the robustness of IKr, defective IKs by blockade of Kv7.1 might produce little AP prolongation in humans and other large mammals190 but might further prolong AP and induce LQT1 when challenged with β‐AR stimulation190 or reduce repolarizing currents by drugs, especially IKr. The gene discussed is KCNQ1; the disease is long QT syndrome 1.