These findings demonstrated that ATS mutations in KCNJ2, which encodes the Kir2.1 channel α subunit, appear to markedly impair its vital role in stabilizing resting membrane potential and mediating the terminal repolarization phase of the action potential, resulting in a predisposition to ventricular arrhythmias through mechanisms discussed below. The gene discussed is KCNJ2; the disease is Andersen-Tawil syndrome.