Muscle atrophy following disuse, disease or denervation leads to an increase in catabolism of muscle proteins through cellular proteolysis [10], achieved with the increased expression of ubiquitin ligases Atrogin-1 (Fbxo32; F-box only protein 32) and MuRF-1 (Trim63; tripartite motif-containing 63), which are regulated by transcription factor Myogenin (Myog) and by class II histone deacetylases (Hdac) [11–14]. Here, MYOG is linked to muscle atrophy.