These results are in contrast to preclinical studies of Duchenne muscular dystrophy gene therapy, which have been hampered by the large size of the dystrophin complementary DNA (cDNA), and attempts to circumvent this by AAV-mediated gene transfer of microdystrophin did not significantly protect hindlimb muscles from contraction-induced injury (8, 15). This evidence concerns the gene DMD and Duchenne muscular dystrophy.