To determine to what extent the full-length dystrophin delivered via lentivirally corrected DMD myoblasts could lead to utrophin reduction, we performed double immunostaining of utrophin (with an antibody that recognizes both mouse and human utrophin) and human dystrophin in sections of DMD-nFLDys, DMD-soFLDys, and normal myoblast-transplanted muscles (Figures 6A–6F and 6a′–6f′) and measured the intensity of the utrophin in human dystrophin+ or human dystrophin− fibers in each section. This evidence concerns the gene DMD and Duchenne muscular dystrophy.