Following acute myocardial infarction (MI), the cardiac autonomic nervous system undergoes a series of structural and neurochemical changes characterized by increased sympathetic drive, heterogeneous patterns of denervation and hyperinnervation, neuronal hypertrophy, altered neurotransmitter signaling within the stellate ganglion, reduced afferent signaling from infarcted myocardium, and a pronounced loss of intracardiac neurons expressing choline acetyltransferase [9,10,11]. The gene discussed is CHAT; the disease is myocardial infarction.