TGFB1 and neuromuscular disease caused by qualitative or quantitative defects of dystrophin: Our previous temporal expression profiling study showed that genes involved in TGF-β pathway were up-regulated at the symptomatic stage of DMD but not differentially expressed at the asymptomatic stage, suggesting that the activation of TGF-β1 pathways was secondary to the primary dystrophin deficiency and may play a critical role in the fibrosis and failure of muscle regeneration in DMD [23].