Moreover, muscles of TnuMDX and TnuE17MDX mice presented metabolic dysfunctions, as determined by the over-expression of pdk4—that coordinates the glucose oxidation and it is over-expressed in patients with a drastic skeletal muscle atrophy75—and GPx1, in accordance with data showed by Messina et al.76 in DMD muscular biopsies. The gene discussed is GPX1; the disease is Duchenne muscular dystrophy.