Aminoglycosides, such as gentamicin, allow the translational machinery to read through these stop codons, thereby producing full-length proteins.53–54 Although a 2-week trial of daily gentamicin in DMD/BMD failed to show dystrophin expression, a 6-month trial of weekly gentamicin demonstrated increased dystrophin expression in DMD boys with nonsense mutations.55–56 Due to dose-limiting toxicities of aminoglycosides, novel agents inducing readthrough have been sought. Here, DMD is linked to Duchenne muscular dystrophy.