Mouse models of impaired dystrophin-DGC function have likewise demonstrated structural abnormalities of the MTJ (Law and Tidball, 1993; Grady et al., 2003) and MRI studies in patients with DMD have demonstrated preferential myocyte loss and replacement fibrosis at the termination of muscle fibers at the MTJs (Nagao et al., 1991). This evidence concerns the gene DMD and Duchenne muscular dystrophy.