In summary, our results show that DMD myoblasts transduced with LV-CK9-soFLDys resulted in higher dystrophin expression in myotubes at both the mRNA level (3.5-fold) and the protein level (around 6-fold) than in the same cells transduced with the same amount of LV-CK9-nFLDys, indicating that sequence optimization of the full-length dystrophin increases the in vivo restoration of the protein. Here, KRT9 is linked to Duchenne muscular dystrophy.