Since the disintegration of the supramolecular dystrophin-glycoprotein complex initiates the multifaceted pathogenesis of dystrophinopathy, which is characterized by highly progressive fibre degeneration, sterile inflammation, fatty tissue replacement and reactive myofibrosis22, it was of interest to study the oligomeric status of a key component of this complex, the integral glycoprotein β-dystroglycan23, in normal versus dystrophic muscles. This evidence concerns the gene DMD and neuromuscular disease caused by qualitative or quantitative defects of dystrophin.