Further, the role of the different STAT5A/B isoforms has recently been addressed, where in a BCR-ABL1-inducible cellular system, knock-down of STAT5B sensitized leukemic cells to imatinib treatment [22] and the attenuation of STAT5A resulted in enhanced basal oxidative stress and DNA damage of normal CD34+ and CML cells as well as growth inhibition of CD34+ cells from patients with acquired imatinib resistance [23]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.