MYBPC1 and arthrogryposis multiplex congenita: We expect this report of two novel mutations (p.P319L and p.E359K) located in C2 domain of MYBPC1 in DA2 patients and our suggestion on the possible molecular mechanisms that may underlie the pathogenesis of DA2 myopathy associated with these two substitutions will stimulate future research to further refine the details of the NH2-teminal interaction of slow MyBP-C with myosin or its other parterners and their importance for myopathy associated with AMC.