While we used a dofetilide-induced model of QT prolongation and ventricular arrhythmia, the cellular mechanisms underlying the antiarrhythmic effects of PDE5 inhibition suggest it may additionally hold antiarrhythmic potential in other conditions causing Ca2+-dependent arrhythmia, such as heart failure (HF), catecholaminergic polymorphic ventricular tachycardia, and digitalis toxicity. The gene discussed is PDE5A; the disease is hydrops fetalis.