Indeed, in a severe Limb Girdle Muscular Dystrophy R1 mouse model (C3KO) that also manifests progressive muscle loss in concert with extensive fibrosis and mitochondrial perturbations consistent with human DMD patients, genetic (follistatin) and pharmacological (anti-myostatin) inhibition of myostatin leads to significant muscle mass gains yet no improvement in strength nor endurance, due to reduced AMPK signalling and consequential loss of oxidative capacity [111]. The gene discussed is MSTN; the disease is Duchenne muscular dystrophy.