One of the factors causing TKI resistance is the cytokine environment that supports growth and survival of CML stem cells irrespective of BCR-ABL activity.[14] In line with this, disruption of the cytokine support in BCR-ABL induced lymphoblastic leukemia enhances sensitivity to imatinib.[36] To further elucidate the function of cytokines in BCR-ABL mediated transformation and leukemogenesis we used SOCS1 as a tool to modulate cytokine signals. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.