Similarly, ∼10% of myonuclei in the H222P mouse model of EDMD (containing a pathogenic point mutation at residue 222 in the lmna gene that causes familial A-EDMD and dilated cardiomyopathy in man) exhibit structural abnormalities and heterochromatin redistribution when examined using muscle sections [41]. This evidence concerns the gene LMNA and dilated cardiomyopathy.