Similarly, El Andari et al. recombined muscle-tropic genomes into chimeric libraries, yielding primary H15/D20/S1/S10 variants; subsequent rational integration of first RGD and then P10 motifs (a tissue specificity enhancer) into these scaffolds generated AAVMYO derivatives with further optimized targeting—AAVMYO2/AAVMYO3 exhibited sharply reduced hepatic/cerebral off-target transduction and effectively alleviated both canine X-linked myotubular myopathy (XLMTM) via MTM1 overexpression and murine DMD via microdystrophin expression [51]. The gene discussed is MTM1; the disease is X-linked myotubular myopathy.