Certain mutations in the dystrophin gene disrupt the reading

frame, leading to little or no dystrophin production and the severe clinical

features seen in Duchenne muscular dystrophy (DMD). However, when the reading

frame is preserved—even if parts of the protein are missing—muscle function is

partially maintained, as observed in Becker muscular dystrophy.

How do antisense oligonucleotide therapies exploit this

difference to improve outcomes in patients with DMD?