To better understand the abnormal processes during skeletal muscle development and regeneration in dystroglycanopathy muscular dystrophy, we performed fiber isotype analysis in two mouse models with conditional knockout of dystroglycanopathy gene Fktn. In the Myf5-cre/Fktn knockout (Myf5/Fktn KO), gene disruption at embryonic day 8 initiates a dystroglycan glycosylation defect during skeletal muscle development, affecting downstream satellite cells and muscle fibers [15]. The gene discussed is MYF5; the disease is muscular dystrophy-dystroglycanopathy.