To see whether the TrJ proteins are maintained in the bigger IDs in DCM heart, we have used immunofluorescence to investigate the distribution of α-actinin and αII spectrin, proteins characteristic of myofibrillar and membranous TrJ, in relation to the CJ and gap junction proteins α- or β-catenin and connexin 43 (Fig. 5). The gene discussed is GJA1; the disease is familial dilated cardiomyopathy.