We thus hypothesize the M-DNM2 is more sensitive to an alteration in the conformational switch of dynamin and that skeletal muscle is more sensitive to CNM mutations, underlying the fact that CNM patients appear specifically affected in skeletal muscle despite the ubiquitous expression of DNM2. Taken together, while the main function of classical dynamins described in cultured cells is vesicle fission in clathrin-mediated endocytosis, the role of DNM2 in muscle may primarily involve other mechanisms in addition to endosome fissioning. This evidence concerns the gene DNM2 and centronuclear myopathy.