One such therapeutic strategy is to overexpress LARGE, a dystroglycanopathy gene (currently associated only with a congenital muscular dystrophy phenotype) that induces hyperglycosylation of α-dystroglycan; this approach has augmented glycosylation in mouse models of two other dystroglycanopathies, FKTN deficiency and POMGnT1 deficiency; these latter two genes have been associated with LGMD as well as congenital muscular dystrophy [128]. This evidence concerns the gene DAG1 and congenital muscular dystrophy.