It is now well established that the lack of dystrophin expression in skeletal and cardiac mdx muscles leads to several secondary processes including inflammation, alteration of intracellular ion homeostasis, chronic degeneration and regeneration and necrosis/apoptosis of muscle fibers, metabolic alterations and interstitial fibrosis all of which exacerbate the progression of DMD [7]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.