Considering that we found a less profound difference in vitro in human myotubes (∼98% of exon 51 skipping giving rise to approximately 48% of dystrophin protein), it cannot be excluded that the discrepancies may be specific or enhanced in the mdx52 model due to the particular genetic engineering of the deletion, since exon 52 has been deleted by gene targeting (i.e., replaced with the neomycin gene),17 as opposed to real deletions at the genomic levels found in DMD patients. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.