Since CML progenitors have recently been described to be particularly dependent on BCL2 for survival and maintenance [4, 5], we evaluated the effectiveness of ABT-199 in reducing the viability of primary CD34+ progenitors from patients in both early [chronic phase (CP)], and advanced stage [accelerated (AP)/blast phase (BP)] CML. The gene discussed is BCL2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.