It has been shown that mutations in myosin, tropomyosin and titin can result in different phenotypes such as HCM, DCM and even arrhythmogenic right ventricular cardiomyopathy (ARVC) and the correlation between a mutation in a particular protein and the disease phenotype is obviously not as clear-cut as initially proposed [74]. This evidence concerns the gene TTN and Arrhythmogenic right ventricular dysplasia.