The cardiac inwardly rectifying potassium current (I_K1) stabilizes the resting membrane potential and is responsible for shaping the initial depolarization and final repolarization of the action potential. The inwardly rectifying potassium channel (Kir2.x) subfamily members primarily mediate cardiac I_K1, but other inward rectifiers, including the acetylcholine-sensitive (Kir3.x) and ATP-sensitive (Kir6.x) inward rectifiers, also may modulate cardiac excitability. Studies suggest I_K1 plays a role in ventricular arrhythmias, highlighted by the recently described Andersen’s syndrome and studies in the guinea pig heart model of ventricular fibrillation. This article describes the salient properties of cardiac I_K1 and discusses the role of this current in the cardiac action potential and in underlying regional differences in cardiac excitability. The mechanism of channel block, assembly, and structure are reviewed. The article discusses the role of I_K1 in ventricular fibrillation and speculates on modulation of I_K1 as a preventative antiarrhythmic mechanism.