The administration of aminoglycosides antibiotics (i.e., Gentamicin, NB54) (Barton-Davis et al., 1999; Politano et al., 2003; Nudelman et al., 2009) and read-through compounds such as RTC13, RTC14 (Kayali et al., 2012), or ataluren (PTC124) (Hamed, 2006; Finkel, 2010) has been proposed as a new strategy to induce ribosomal read-through of premature termination mutations, to obtain a full-length dystrophin protein in patients with DMD and Becker Muscular Dystrophy (BMD) (Figure 2). This evidence concerns the gene DMD and Duchenne muscular dystrophy.