AKT1 and neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan: To determine whether Akt/mTOR signaling is altered in dystroglycanopathy mice, we examined the activation status of pathway proteins in fasted Myf5/Fktn KO muscle from mice aged 17–25 weeks, an age range with substantive remodeling of the muscle compartment.