Direct evidence for the ability of utrophin to functionally compensate for dystrophin deficiency comes from experimental studies in animal models of DMD demonstrating that utrophin over-expression driven by transgenic means, viral vectors, pharmacological promoter activation or protein transduction can rescue dystrophin-deficient muscle in mice and dogs [7], [8], [9], [10], [11], [12], [13]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.