SLC2A1 and acute lymphoblastic leukemia: Conversely, inhibition of BCR-Abl in leukemic cells suppresses glucose uptake and glycolysis.4, 5, 6, 7 This regulation of glucose metabolism may be critical for survival of BCR-Abl B-ALL, as enforced expression of Glut1 protected B-ALL cells from imatinib-induced apoptosis.8 These data show that BCR-Abl promotes glucose uptake and aerobic glycolysis, and BCR-Abl-transformed cells may rely on this pathway.