Specifically, the most severe mutant Arg975Trp is associated with both dilated (DCM) and hypertrophic (HCM) cardiomyopathies in man where it disrupts the organization of intercalated discs, results in a pI drop of about 1.4 pH units for residues 966–983, augments cross-linking of actin filaments [8], and may compromise the interactions of metavinculin with its partners, including vinculin [9]. This evidence concerns the gene VCL and familial dilated cardiomyopathy.