This observation is in agreement with previous studies demonstrating a BCL-XL dependence of stem cell survival for human embryonic stem cells as well as non-small-cell lung cancer cells.35, 36 Thus, targeting BCL-XL potentially offers great therapeutic benefits in CML, especially due to the insensitivity of quiescent CD34+ progenitor CML cells to imatinib, which is a major factor in the recurrence of the disease on discontinuation of therapy,17, 37 although it will be necessary to overcome potential toxicities, such as thrombocytopenia, associated with BCL-XL inhibition.22, 38. The gene discussed is BCL2L1; the disease is Thrombocytopenia.