Identifying the molecular determinants of DCM and morphological characteristics in these mice allows for opportunities to understand and potentially pharmacologically treat the pathology in both Lmna−/− and Lmna+/− mice, with extensions to understanding how DCM develops in humans with LMNA mutations, which typically appear as autosomal dominant heterozygous mutations. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.