Splice site mutations in the DMD gene have been reported to result either in DMD, BMD or intermediate phenotypes in humans (Sironi et al. 2001; Adachi et al. 2003; Thi Tran et al. 2005; Takeshima et al. 2010; Magri et al. 2011), and DMD-like disease in the naturally occurring golden retriever (GRMD) canine model of DMD that arises from a single base change affecting the dystrophin exon 7 acceptor splice site (Sharp et al. 1992). This evidence concerns the gene DMD and Duchenne muscular dystrophy.