These observations suggest that molecular interactions and effects of various DCM mutants converge to a depressed contractile phenotype at the cellular level due to alterations in (a) calcium sensitivity of myofilaments, (b) thin-filament activation, (c) maximal ATPase activity, (d) in-vitro motility (e) calcium affinity of Tn and (f) mechano-transduction, thereby triggering the signaling mechanism leading to DCM (Chang and Potter, 2005; Lakdawala et al., 2012b). Here, DNAH8 is linked to familial dilated cardiomyopathy.