The t(9;22) chromosomal translocation that generates the oncogenic kinase BCR-Abl occurs in ~25% of adult B-cell acute lymphoblastic leukemia cells (B-ALL) and is associated with poor prognosis.2 The metabolic program of B-ALL cells is undefined, although diffuse large B-cell lymphoma (DLBCL) can either be highly glycolytic or use oxidative phosphorylation and mitochondrial metabolism.3 It has been suggested that BCR-Abl signaling is associated with elevated glucose metabolism, as BCR-Abl can promote glucose uptake and trafficking of glucose transporter Glut1 to the cell surface. The gene discussed is BCR; the disease is precursor B-cell acute lymphoblastic leukemia.