These include reducing the colony-forming capacity of CP-CML progenitors (CD34+ CP-CML cells, venetoclax with imatinib)80, reducing leukemic burden and long-term engraftment potential and increasing overall survival in CML murine models (Bcr-Abl1+ Tet-off Lin-Sca-1+cKit+ cells, venetoclax with nilotinib)35, and increasing apoptosis in BP-CML progenitors (CD34+CD38− BP-CML cells, venetoclax with nilotinib)35, (CD34+ BP-CML cells, ABT-737 with imatinib)81 and CP-CML progenitors (CD34+CD38- CP-CML cells, ABT-737 with imatinib/nilotinib)82. The gene discussed is KIT; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.