An important corollary to the recent advances in our understanding of the primary cause of Duchenne muscular dystrophy^1–6, is the validation of genuine genetic homologues as animal models of the disease^7,8 in which potential therapies can be tested. The persistent skeletal muscle necrosis that characterizes human Duchenne muscular dystrophy⁹ is also seen in the mdx mouse^10–13 and is, in both, a consequence of a deficiency of dystrophin^6,7, probably within the muscle fibres themselves^14–16. As injected muscle precursor cells of one genotype can fuse with host muscle fibres of a different genotype and express the donor genes^17,18, we decided to test grafts of normal muscle precursor cells to see if they could induce synthesis of dystrophin in innately dystrophin-deficient mdx muscle fibres. We show that injected normal muscle precursor cells can fuse with pre-existing or regenerating mdx muscle fibres to render many of these fibres dystrophin-positive and so to partially or wholly rescue them from their biochemical defect.