Furthermore, as TKI-resistant mutations are produced by large levels of ROS accumulated by imatinib-treated CML-CP leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs), antioxidant therapy may be used in conjunction with TKIs to increase or prolong the therapeutic benefits of ABL1 kinase inhibitors. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.