Gene replacement therapies utilizing adeno-associated viral vector delivery of truncated versions of dystrophin (mini- and microdystrophins) hold great potential for the treatment of Duchenne muscular dystrophy (DMD). However, these truncated dystrophins are not fully functional and episomal AAV vectors are not permanently retained following delivery to muscle. A more long-lasting and effective approach to gene therapy could result from methods to modify the dystrophin gene using gene editing strategies. The CRISPR/Cas9 system has been shown to be a highly specific method for genetic modifications, and recently has been proven applicable to correct mutations responsible for DMD. Here we present in vivo approaches for targeted correction of the dystrophin gene in the mdx4cv mouse model of DMD using both single- and dual adeno-associated viral (AAV) vector delivery systems of Cas9 and DMD mutation specific targeting guide RNA's. Treated muscles demonstrated successful targeting of the dystrophin gene leading to a corrected open reading frame in the messenger RNA resulting in a restoration of near-to full-length dystrophin expression in up to 70% of treated muscle cross-sectional area. These results demonstrate that successful in vivo dystrophin correction can be achieved following AAV mediated delivery of CRISPR/Cas9, showing promise for the development of future clinical application of technologies for permanent correction of mutations leading to DMD and other genetic muscle disorders.