Moreover, Dmd Δ52-54 mice could be utilized as an informative dystrophin-deficient model for mutation-independent strategies, such as upregulation of utrophin or other DMD disease modifiers (van den Bergen et al., 2015; Vo and McNally, 2015; Weir et al., 2004; Wojtal et al., 2016). This evidence concerns the gene UTRN and Duchenne muscular dystrophy.