DMD is caused by loss-of-function mutations in the gene encoding dystrophin (DMD), which performs structural and signaling functions at the sarcolemma.1, 2, 3 The leading approach for treating DMD is exon skipping, whereby splicing of the DMD pre-mRNA is modulated using antisense oligonucleotides, such that the translation reading frame is corrected, and an internally truncated, partially functional quasi-dystrophin protein is produced.4 Here, DMD is linked to Duchenne muscular dystrophy.