In this study, we have demonstrated the application of antisense therapy to induce skipping of exon 51 in CKCS-MD and restore dystrophin expression: the identical approach (skipping the same exon) has the potential to restore the reading frame and produce functional dystrophin and improved clinical signs in more DMD patients than with any other site (up to 13% of DMD patients) [11], [12], [15]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.