Microarray analysis of CD34+ CML progenitor cells exposed to hypoxia revealed increased expression of cell adhesion and survival genes, concordantly with decreased apoptosis and improved colony-forming potential, thereby suggesting that targeting HIF1α along with BCR-ABL may represent a therapeutic opportunity for eradication of LSCs in CML patients (85). This evidence concerns the gene HIF1A and chronic myelogenous leukemia, BCR-ABL1 positive.