TKI treatment leads to dynamic alterations in glycolysis and OXPHOS in CML progenitors. (A) Overall experimental strategy. BM cells (2 × 10⁶) from BCR-ABL transgenic mice (CD45.1/2) in which leukemia had been induced by tetracycline withdrawal were transplanted into CD45.1 recipient mice. Once mice had developed leukemia 6 or 8 weeks after transplantation, they were treated with nilotinib (TKI) or vehicle for 2 days or 2 weeks. BM c-Kit⁺ cells and LSK cells were selected and studied as shown. (B-C) Extracellular flux analysis of OCR (B) and ECAR (C) in CML BM c-Kit⁺ cells after 2 days of nilotinib treatment (n = 4 mice each). (D-E) Extracellular flux analysis of OCR (D) and ECAR (E) in CML BM c-kit⁺ cells after 2 weeks of nilotinib treatment (n = 5-6 mice each). Significance values: ∗P < .05; ∗∗P < .01; ∗∗∗P < .001. Results represent the mean ± standard error of mean (SEM) of multiple replicates.