Although this suggests that the effect of hyperglycosylation strategies might need to be evaluated carefully, it is important to acknowledge both that the deficit was only subclinical and also that the transgenic overexpression of LARGE in a normal muscle differs radically from the situation in a muscle depleted of glycosylated α-DG epitopes, such as in the dystroglycanopathies, where the absence of a proper α-DG-laminin interaction plays a major pathogenic role. Here, LARGE1 is linked to neuromuscular disease caused by qualitative or quantitative defects of alpha-dystroglycan.