The transgenic overexpression of SSPN in mdx mice, a murine model of DMD, increases the abundance of the compensatory ECM receptors—the UGC and α7β1–integrin complex—at the myofiber membrane [12]; increases the C-type 2 glycosylation of α-DG [13]; and enhances laminin binding [12,14,15]. This evidence concerns the gene LAMB2 and Duchenne muscular dystrophy.