Thus, in the present study, we further hypothesized that in congenital myopathies due to RYR1 mutations, aberrant PTMs on MyHCs would be associated with an increase in the proportion of myosin molecules in the disordered–relaxed state, thereby impairing the ATP demand of resting myofibres and indirectly explaining some of the myopathic phenotypes. The gene discussed is MYH14; the disease is congenital myopathy with cores.