LMNA+/− heterozygous knockout mice showed 50% normal cardiac lamin AC levels, along with age-dependent development of atrioventricular nodal myocyte abnormalities (nuclear shape alterations and active apoptosis), AV conduction defects, impaired cardiomyocyte contractility, and DCM, revealing that lamin AC haploinsufficiency causes DCM with conduction system disease in mice [34,35]. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.