The rationale for this strategy relies on the following facts: (1) utrophin is a paralog of dystrophin; (2) it is capable of replacing dystrophin as an anchor of sarcolemma to the cortex cytoskeleton; (3) it is non-immunogenic when overexpressed, in contrast to dystrophin, which may be recognized as a foreign protein by the immune system of DMD patients; and (4) it is potentially useful regardless of a patient’s DMD mutation. The gene discussed is UTRN; the disease is Duchenne muscular dystrophy.