Our previous work demonstrated that CML stem and progenitor cells that are TKI-resistant, but lack explanatory BCR-ABL1 kinase domain mutations, are dependent on the activation of alternative signaling pathways, especially signal transducer and activator of transcription 3 (STAT3) [19–21]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.