TNNT2 and atrial fibrillation: Previous studies on I79N, F110I, R278C TNNT2 mutations (all hot-spot sites for AF, according to our analysis in HCM patients) clearly demonstrated that increased myofilament Ca2+-sensitivity, by modifying cytosolic Ca2+ buffering, promotes DADs and triggered activity (Schober et al., 2012), representing a direct cause of arrythmias in both atrial and ventricular cardiomyocytes.