For example, improving engraftment efficiency at a site of inflammation by overexpressing the pro-survival gene AKT serine/threonine kinase 1 (Akt1) [13], or endowing hMSCs with new therapeutic properties, such as expressing the full length dystrophin gene in hMSCs for Duchenne muscular dystrophy therapy [14]. This evidence concerns the gene AKT1 and Duchenne muscular dystrophy.