With respect to the therapeutic benefit of myostatin inhibition, Parsons et al. [42] reported that elimination of myostatin can improve the dystrophic phenotype in mice nullizygous for δ -sarcoglycan (scgd-/-) (a model of human limb-girdle muscular dystrophy referred as LGMD2F). The gene discussed is MSTN; the disease is autosomal recessive limb-girdle muscular dystrophy type 2F.