For instance, M531R mutants in the motor domain of the human β/slow-cardiac myosin molecule have been shown to be stronger motors and have been suggested to interrupt myosin head putative interactions with other proteins (eg, myosin-binding protein C) resulting in hyperdynamic heart.18 In contrast to congenital cardiomyopathies where a vast number of mutations have hypercontractile consequences, most of skeletal myopathies-related mutations induce hypocontractility and overall weakness,17, 19–21 with only a few exceptions contributing to muscle stiffness and/or hypertonia.22, 23. Here, MYH14 is linked to Skeletal myopathy.