However, in tamoxifen-inducible Fktn KO mice, factors related to Akt/mTOR signaling were unchanged before the onset of dystrophic pathology, suggesting that Akt/mTOR signaling pathway abnormalities occur after the onset of disease pathology and are not causative in early dystroglycanopathy development. The gene discussed is AKT1; the disease is neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.