Atrial fibrillation is mediated by an increased sensitivity to β1 adrenergic receptors and decreased sensitivity to M2 muscarinic receptors [14], decreased L-type calcium channel activity, increased automaticity in pulmonary vein myocytes with a rise in arrhythmogenicity [15], and increased voltage-gated potassium channel activity with the latter shortening the refractoriness of myocytes, enhancing re-entry circuits [16]. Here, CHRM2 is linked to atrial fibrillation.