Indeed, deletion of HIF1α within the osteoblast lineage decreased bone.(51) Alternatively, the deletion of PHDs or von Hippel‐Lindau proteins that drive HIF degradation within the osteoblast lineage increased bone volume and density likely because of the constitutive activation of HIF transcription factors.(52, 53, 54) Iron deficiency is also known to enhance HIF1α accumulation as iron, in addition to oxygen, is a critical cofactor for PHD activity.(55) HIF1α protein was stabilized in the hMSCs in a DFO dose‐dependent manner during osteoblast differentiation. The gene discussed is HIF1A; the disease is Iron deficiency anemia.