Incubation of Chronic Myeloid Leukemia (CML) cells in hypoxia, including K562 as well as the corresponding primary cells (from blast-crisis patients), results in the complete suppression of BCR/Abl protein, but not mRNA, so that hypoxia-selected CML stem cells, while remaining genotypically leukemic, are phenotypically independent of BCR/Abl signaling and thereby refractory to the treatment with Imatinib-mesylate (IM) [1], [3]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.