In chronic myeloid leukemia (CML), which is driven by the oncogenic tyrosine kinase BCR-ABL, GSK-3 was reported to be inactivated and enforced expression of constitutively active GSK-3 reduced proliferation and potentiated BCR-ABL inhibitor–induced apoptosis in both BCR-ABL inhibitor–sensitive and -resistant cells (55). Here, ABL1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.