Importantly, dystrophin deficiency seems to be naturally alleviated by expression of the utrophin (UTRN) gene in both humans and animal models [37, 38], which is signified by the structural and functional similarities between utrophin and dystrophin [39, 40] and by the differences in the severity of the phenotype of various DMD mouse models. The gene discussed is UTRN; the disease is Duchenne muscular dystrophy.