Therefore, since DUX4 expression activates embryonic genes and the embryo metabolism is predominantly glycolytic, abnormal activation of glycolysis through HIF1α could contribute to metabolic disturbances in FSHD muscle cells, specifically in myotubes that rely on OXPHOS much more than myoblasts. The gene discussed is HIF1A; the disease is facioscapulohumeral muscular dystrophy.