Given the central role of STAT3 in regulating metabolic pathways in various cancers and its role with ZFAS1 mentioned above, we hypothesize that ZFAS1 may modulate STAT3 activation or function, thereby contributing to imatinib resistance in CML through the reprogramming of glucose metabolism. Here, ZFAS1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.