Nemaline myopathy (NM) is a non-dystrophic congenital myopathy. The hallmarks of this disorder are early onset weakness, hypotonia, skeletal deformities and rod-like inclusions within the sarcolemma of muscle cells. Several gene mutations have been identified in NM. Of these, a non-sense mutation in the TNNT1 gene (encoding for the slow skeletal muscle isoform of troponin T) results in a selective atrophy of slow-twitch myofibers and in a fatal form of NM named Amish Nemaline Myopathy (ANM). There is no treatment for ANM, but the development of an AAV gene therapy is viable and explored in our study. Such an approach requires restricting the expression of TNNT1 to slow-twitch myofibers, thus avoiding deleterious effects associated with the presence of this protein in cardiac cells and fast-twitch myofibers. We accomplished high efficiency muscle transduction and myofiber-type specificity using microRNA de-targeting techniques.