Functionally, while the direct functions and mechanisms of theANK2 variants were not explored, the researchers observed severe cardiacabnormalities characteristic of ACM in the ANK2-cKO mouse model, agenetically engineered model with cardiomyocyte-specific deletion of ankyrin-B.These abnormalities primarily included biventricular dilation, reduced ejectionfraction, cardiac fibrosis, premature death, sinus bradycardia, QTc intervalprolongation, and catecholamine-induced ventricular arrhythmias. Here, ANK2 is linked to Sinus bradycardia.