While greater than 90% of RYR2 mutations discovered to date are missense mutations, heterozygous CNVs involving the in-frame deletion of RYR2 exon 3 (35 amino acids, Asn57_Gly91) that also leads to an overall GOF of RyR2 have been reported to cause a wide spectrum of clinical phenotypes, including autosomal dominant CPVT1, sinoatrial node dysfunction, bradycardia, atrial fibrillation, atrioventricular block, dilated cardiomyopathy, left ventricular noncompaction, and SCA (3, 8–11). This evidence concerns the gene RYR2 and Bradycardia.