TTN and familial dilated cardiomyopathy: Two nonmutually exclusive hypotheses have been developed to explain DCM pathogenesis for TTNtvs, namely, haploinsufficiency and “poison peptide.” Full-length TTN is decreased in TTNtv DCM hearts compared with non-TTNtv DCM hearts, and truncated TTN proteins have been shown to incorporate into sarcomeres in patients with DCM (11–14).