Given that even culturing MDS CD34+ cells in 21% FiO2, which is an oxygen supply way over that of both the control and MDS BM, did not suffice to degrade HIF-1α (Figure 6), we strongly argue toward a non-canonical pathway of intracellular dysfunction driving the over-tuned HIF-1 activity and therefore will further discuss our theories as future experimental and subsequently therapeutic targets. The gene discussed is HIF1A; the disease is myelodysplastic syndrome.