It is not yet clear whether the dysregulated gene expression in FSHD myoblasts is due to disease-related differences in transcription regulatory or RNA-processing proteins, cell signaling (e.g., TGFβ or RHO/mTOR pathways [64,65]), indirect effects on transcription from overexpression of extracellular proteins [66], indirect effects of mitochondrial dysfunction [67], subtle differences in timing of expression of some myogenesis-specific gene(s), and/or disease-specific epigenetic differences. This evidence concerns the gene MTOR and facioscapulohumeral muscular dystrophy.