AKT1 and neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan: In another study, disrupting the interaction between αDG and laminin was found to induce apoptosis and reduce Akt phosphorylation [37] while treatment of a fukutin-deficient dystroglycanopathy with the mTOR inhibitor RAPA was found to increase myofiber size [38].