The “proof-of-principle” of such a strategy has been demonstrated by the ability of utrophin to compensate for the deficiency of dystrophin in the dystrophin-deficient mouse muscle [46], and by the ability of ε-sarcoglycan to compensate for the lack of α-sarcoglycan in autosomal recessive limb-girdle muscular dystrophy type-2D [47]. This evidence concerns the gene UTRN and autosomal recessive limb-girdle muscular dystrophy type 2D.