Importantly, the concurrent buildup of proNGF/p75NTR protein levels in mdx muscles, together with the increase in ngf/ngfr transcripts in DMD patients, suggest that the hyperactivation of the proNGF/p75NTR pathway could counteract the establishment of the slow/oxidative phenotype in the dystrophic pathology, in a similar fashion to that observed in SCDMs. The gene discussed is NGFR; the disease is Duchenne muscular dystrophy.