Shinohara et al. reported that inactivation of BCR-ABL by the tyrosine kinase inhibitor imatinib strongly suppressed glycolysis and a compensatory increase of FAO by up-regulating CPT1C in Ph-positive ALL and chronic myeloid leukemia (CML) cells. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.