Furthermore, mouse studies have provided evidence that MPO can contribute to cardiac remodelling and also myocardial fibrosis, and MPO deficiency could preserve cardiac function, and reduce atrial fibrillation and ventricular tachycardia under pro-fibrotic conditions, present in severe heart failure models, like in post-myocardial infarction30–33. The gene discussed is MPO; the disease is ventricular tachycardia.