Proliferation, self-renewal and viability of CML cells were drastically impeded by pharmacological interference with EZH2 activity (GSK126 inhibitor), or by reducing its expression through shRNA or in Ezh2−/− CML mice, resulting in increased survival in retroviral BCR-ABL1-transduced mouse models [66,68]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.