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Our work has shown that by catalyzing tubulin and Smad3 deacetylation, HDAC6 respectively regulates acetylcholine receptor distribution and TGF signaling in muscle fibers, thereby controlling muscle mass and neuromuscular junction organization. Further investigation of HDAC6 in Duchenne Muscular Dystrophy and Spinal Muscle atrophy revealed new potential strategies of pharmacological treatment based on HDAC6 inhibitors for neuromuscular disorders. Altogether, our aim is to further understand the role of HDAC6 in skeletal muscle cells and develop the use of HDAC6 inhibitors in neuromuscular disorders.