PDE4D, a member of phosphodiesterases predominantly expressed in atrial myocytes, regulates cyclic adenosine phosphate levels and Ca2+ influx/release in atria, thereby preventing atrial arrhythmias.[42] Studies have shown the correlation between RLN2 and AF, with RLN2 inhibiting atrial fibroblast migration, reducing inflammation, and exerting protective effects against AF.[43] Additionally, RLN2 is a candidate drug for acute HF, enhancing myocardial contractility.[44]. The gene discussed is PDE4D; the disease is atrial fibrillation.