Thus, the absence of dystrophin is associated with intracellular Ca2+ and Na+ overload in DMD patients [9] and mdx mice [10], [11], alterations in transient receptor potential channel function (TRPC) [12] and activation of several Ca2+-dependent intracellular signaling pathways in skeletal muscle [10], [11], [13]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.