ASO therapies that skip one or two exons can have the potential to treat 83% of DMD patients (79% of all patients with deletions, 73% of all patients with duplications, and 91% of all patients with small mutations), but that leaves 17% of patients with mutations in essential dystrophin protein-coding regions without ASO therapies [40]. This evidence concerns the gene DMD and Duchenne muscular dystrophy.