Dystrophin splice site mutations have been relatively neglected as targets in DMD therapeutic exon skipping studies, despite reports that splice motif changes cause at least 15% of all mutations in human inherited disease (Krawczak et al. 1992) and in an early study, 7% of DMD/BMD cases (Roberts et al. 1994). This evidence concerns the gene DMD and Becker muscular dystrophy.