UTRN and Duchenne muscular dystrophy: On other hand, in addition to the miR-206 effect on myoblast differentiation mentioned above, Bulaklak et al showed that the AAV-mediated inhibition of miR-206, another miR dysregulated in DMD, in the muscles of dystrophic mdx mice increases the expression of compensatory “booster genes” in DMD, such as VEGFA and utrophin, thus improving motor function and reducing muscle fibrosis [132] (Table 3).