Mouse models generated to investigate the molecular and cellular pathogenesis of LMNA-DCM include knock-in mice ubiquitously expressing Lmna mutations homologous to those that cause the disease in humans (LmnaN195K/N195K and LmnaH222P/H222P) and knock-out mice with whole body Lmna deficiency, which progressively develop cardiac fibrosis and conduction defects and DCM and die prematurely [18,19,20,21]. This evidence concerns the gene LMNA and fibrosis.