The current molecular view of dystroglycanopathies implies that the observed reduction in sarcolemma stability would originate from the reduction of the binding affinity displayed by α-DG towards laminin, an event whose molecular basis is represented by an alteration of the O-mannosylated α-DG moieties and not by its dramatic hypoglycosylation. The gene discussed is LAMB2; the disease is neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.