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. This evidence concerns the gene MYF5 and neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.