The findings highlight the contribution of cardiac fibroblasts to the pathogenesis of LMNA-associated DCM, as the deletion of the Lmna gene in fibroblasts leads to cardiac dilatation and dysfunction, cardiac arrhythmias, myocardial fibrosis, and apoptosis, a phenotype that resembles that of the DCM. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.