In both lamin A/C-deficient (LMNA−/−)[16] and lamin A/C-insufficient (LMNA+/−)[18] mouse models, animals were born with normal functioning hearts, but eventually developed premature cardiac aging with various degree of atrioventricular block, atrial arrhythmias, DCM, and ventricular tachycardia, closely resembling to those observed in humans with heterozygous LMNA mutations. The gene discussed is LMNA; the disease is familial dilated cardiomyopathy.