The crucial role of HIF1α in promoting maintenance of CML LSCs was also validated in a BCR-ABL transgenic mouse model, where HIF1α conditional deletion resulted in impaired LSCs propagation caused by delayed proliferation and induction of apoptosis via expression of p16Ink4a, p19Arf and p53 (86). The gene discussed is HIF1A; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.