This is an antibiotic that has figured prominently in recent news items about cases of Duchenne due to premature "stop codons." In these cases the complete gene for dystrophin is never "decoded" or translated so that this critical muscle protein is not made, or at least not made in full form. Research on mdx mice that simulate human Duchenne has shown that when gentamycin is administered, the premature stop codon is somehow ignored so that the entire gene transcript can be "read" and dystrophin can be produced. A preliminary trial on Duchenne young men is underway, and hopes are high that this will work in humans as well as it did in the model mice. Unfortunately, this treatment would only work for those instances (about 10% of all Duchenne cases) in which the gene defect is a premature stop codon.