In this regard, it was suggested that DCM is a disease of “loose sarcomeres.” In clear contrast, HCM-causing mutations in TCAP increase the binding of Tcap to titin and calsarcin-1 [52], leading to a hypothesis that HCM may be a disease of “stiff sarcomeres” [56]. The gene discussed is TTN; the disease is familial dilated cardiomyopathy.