More in general, the development of DCM in dystrophin-deficient tissues is caused by the remodeling of ECM that leads to dysfunctions in the collagen fibrils that transmit the contractile force and alterations in other ECM proteins (as fibronectin and glycoproteins) and in cell-matrix interactions: all together, these pathological cues cause the rising of fibrosis and the impairment of cardiac functionality. The gene discussed is DMD; the disease is familial dilated cardiomyopathy.