Atrial fibrillation caused a significant increase in the relative amount of the slow β-HC expressed by the human atrial myocardium compared to control conditions (from 10–25% to 40–50%, [141]) which could directly account for the observed marked reduction in activation and relaxation kinetics observed in the myofibrils from atrial fibrillation patients [31], in association with the parallel shift of LC1 and LC2 expression from the ventricular to atrial forms [49, 50]. This evidence concerns the gene NKX2-1 and atrial fibrillation.