In imatinib-resistant chronic myeloid leukemia (CML), transformed BCR-ABL inhibited TXNIP transcription by inducing c-Myc and initiated a glucose-dependent survival program, while the overexpression of TXNIP or the TXNIP agonist JQ1 inhibited the activity of the key enzymes hexokinase 2 (HK2) and lactate dehydrogenase A (LDHA), thereby synergizing with imatinib to kill CML cells and demonstrating the link between TXNIP and metabolism [210]. This evidence concerns the gene HK2 and chronic myelogenous leukemia, BCR-ABL1 positive.