Treatment with Trichostatin A (TSA) can improve morphology and function of skeletal muscle in mdx mice via the upregulation of follistatin [8], and valproic acid can improve muscle integrity and function in the mdx/Utrophin−/− double mutant mouse model of DMD via activation of the Akt pathway [9], however these compounds are yet to be tested in humans. This evidence concerns the gene AKT1 and Duchenne muscular dystrophy.