Furthermore, disruption of endogenous myostatin by gene or RNA targetings was shown to result in anatomic, biochemical, and physiologic improvements in the dystrophic phenotype of mdx mice, a mouse model of DMD with a nonsense mutation in the dystrophin gene [21,22], including particularly prominent enlarged fiber diameters and greatly reduced fatty fibrosis. This evidence concerns the gene DMD and Duchenne muscular dystrophy.