Although the exact pathophysiological mechanisms involved in NT-proBNP release in AF are less clear, it has been suggested that its secretion from the atrial myocytes could be induced by gene upregulation [33] and atrial remodeling due to electrical changes (high atrial rates, shortening of atrial refractory period, increased conduction velocity and ionic alterations) and hemodynamic stressors (atrial overload, stretch and fibrosis) [34,35]. The gene discussed is NPPB; the disease is atrial fibrillation.