If one considers a putative pathological contribution of HIF1α to FSHD, it is noteworthy that HIF1α promotes a metabolic switch in favor of anaerobic glycolysis, the metabolic pathway favored in early embryogenesis, where DUX4 and mouse Dux have a function in zygotic genome activation [9,10,41]. This evidence concerns the gene DUX4 and facioscapulohumeral muscular dystrophy.