Overall, these recent studies have underlined the critical role of hypoxia and H1F-1α, altered metabolic pathways and autophagy for the survival and treatment resistance of LSCs in the hypoxic microenvironment of BM, including in the insensitivity of BCR-ABL+ CML-LSCs to TKIs that target the bulk mass of proliferative leukaemic cells. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.