Previous studies have shown that ANS dysfunction provides substrates for atrial arrhythmias, and modulation of ANS activity has been recognized as a promising strategy for the treatment of AF.36 In particular, we discovered a significant increase in the levels of TH and GAP43, which revealed a higher degree of nerve growth and confirmed augmented sympathetic control in CUS-induced rats. The gene discussed is GAP43; the disease is atrial fibrillation.