In line with these findings, a metabolic profile of CD34+ and CD34− chronic myeloid leukemia (CML) cells, derived from fourindividuals by recording steady-state levels of 70 metabolites through liquid chromatography–mass spectrometry (LC–MS), highlighted a selective increase in glucose oxidation and anaplerosis, the process of replenishment of depleted metabolic pathway intermediates, in CML cells resistant to imatinib treatment [105]. This evidence concerns the gene CD34 and chronic myelogenous leukemia, BCR-ABL1 positive.