Although the prolonged action potential duration may have acted to inhibit atrial fibrillation at an early age in the AMPK-dKO mice, reduced repolarizing currents might have been arrhythmogenic later in this model by inducing early atrial afterdepolarizations, action potential alternans, or the dispersion of repolarization (30). The gene discussed is PRKAA1; the disease is atrial fibrillation.