For instance, KCNQ1 mutations lead to a gain-of-function in the IKs channel complex, which increases the repolarizing K+ current, shortens the action-potential duration (APD) and the atrial refractory period and, in turn, renders the cells susceptible to depolarization by subsequent AF triggers in the form of electrical impulses. The gene discussed is KCNQ1; the disease is atrial fibrillation.