MTM1 and centronuclear myopathy: They came to a similar conclusion in their work with an experiment in mice after administration of rAAV8 [102], short-term replacement of myotubularin with a prototypical targeted protein replacement agent (3E10Fv-MTM1) [103], or used the selective inactivation of PI3KC2β kinase activity [104], which improved contractile function and muscle pathology, and thus is associated with a highly promising treatment potential for myotubular myopathy.