This alternative gene therapy strategy for Duchenne muscular dystrophy (DMD) targets exon 10 of the DMD gene. A previously developed AAV‑U7snRNA exon‑2 skipping vector was able to successfully restore full‑length dystrophin expression in a mouse model of exon‑2 duplication and has since advanced into clinical trials with promising preliminary results. To hold on that research, this new model uses AAV constructs carrying antisense sequences targeting exon 10 of the DMD gene, delivered under the control of a mouse U7 promoter. These constructs have been tested in DMD patient‑derived FibroMyoD cell lines, demonstrating effective targeting of exon 10 with the goal of restoring an open reading frame and reestablishing expression of either full‑length or partially functional dystrophin. Thus serving as an alternative to micro‑dystrophin therapies and further expands the therapeutic potential of U7snRNA‑based exon skipping for a broader spectrum of dystrophin mutations.