The Largemyd mouse model of dystroglycanopathy, in which there are defects in the glycosylation of α-dystroglycan (a component of the dystrophin-associated glycoprotein complex) (Muntoni et al, 2004), has significantly more satellite cells than wild type control muscles, at 2–3 months of age (Ross et al, 2012). The gene discussed is DAG1; the disease is neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.