Mutations that generate a premature termination codon (PTC), either via point mutation (such as in the classic animal model of DMD, the mdx mouse [28,29]) or through frameshift following the deletion or duplication of one or more exons, result in essentially no detectable dystrophin protein and, consequently, a DMD phenotype (notably, 7 of the 10 exons within the 44–53 region are vulnerable to frameshift). Here, DMD is linked to Duchenne muscular dystrophy.