For example, in a family with XL-DCM with a missense mutation in exon 29, there was a decrease in dystrophin up to 20% of normal in skeletal and cardiac muscle; however, β- and δ-sarcoglycans were clearly decreased in sarcolemma of the cardiac muscle but not in the skeletal muscle tissue, showing that molecular changes in dystrophin yielding structural changes within the protein may disrupt dystrophin-associated proteins [80]. This evidence concerns the gene DMD and familial dilated cardiomyopathy.