While mutations in sarcomeric proteins associated with canine DCM have not been reported, the phenotypic similarities in myofilament dysfunction between human and canine DCM provides strong support for their use as comparative models to identify the molecular basis of DCM in terms of contractile dysfunction, and to test myofilament-targeting therapies like small molecules that promote myosin activation [109]. This evidence concerns the gene MYH14 and familial dilated cardiomyopathy.