DMD and Becker muscular dystrophy: Mutations that cause premature termination of dp427 result in DMD, however mutations that cause in-frame internal truncation of dp427 typically lead to the milder condition, Becker muscular dystrophy (BMD), suggesting that while N and C termini are critical for function, the rod domain is largely dispensable: indeed, use of antisense oligonucleotides to mask splicing sites in the dp427 pre-mRNA leads to omission of targeted exons in DMD-causing transcripts and consequent restoration of reading frame, offering a means to change DMD to a BMD phenotype.