To determine whether known molecular mediators of ventricular repolarization defects and arrhythmia were affected by PEPs, we assessed protein expression of voltage-gated potassium channels key to ventricular repolarization (Kv1.5, Kv4.2, Kv4.3, and Kv7.1) at 10 weeks post-PEPs [58–60]. The gene discussed is KCND2; the disease is Arrhythmia.