In contrast, deletion of Jak2 or Stat5 in IM-sensitive and IM-resistant Bcr-Abl+ cells resulted in reduced colony formation and apoptosis [41]; therefore, Jak2/Stat5 inhibitors may be useful for CML therapy and the combination of TKI with CM363 might offer advantages to circumvent resistance to direct Bcr-Abl inhibitors. The gene discussed is STAT5B; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.