Chronic myelogenous leukemia (CML) is a hematological malignancy that expresses the BCR–ABL fusion oncogene. It has three distinct clinicopathological phases: chronic phase, accelerated phase and blast crisis. Tyrosine kinase inhibitors, which target the BCR–ABL fusion protein, can induce complete cytogenic remission in more than 70% of newly diagnosed chronic CML patients. However, complete molecular response is a rare event in these CML patients with complete cytogenic remission, suggesting that they are not effective in eliminating CML leukemia-initiating cells (LIC), although there are differences between the trosine kinase inhibitors. Once CML progresses to blast crisis, it becomes resistant to most treatment approaches, and survival rapidly declines. The exact underlying mechanism of transformation of chronic phase CML to blast crisis is still unclear; however, it is thought to be supported by self-renewing LIC. Therefore, identifying genes or signaling pathways involved in the self-renewal of LIC may promote more effective leukemia treatments. So far, two key regulators in self-renewal of LIC have been linked to CML progression, Wnt/β-catenin and Bmi-1. 1–4

Recently, several research groups, including ours, have demonstrated that SALL4 has an essential role in the maintenance of pluripotent and self-renewal properties of embryonic stem cells by interacting with Nanog and Oct4. 5 In addition, our group has shown that constitutive expression of SALL4 contributes to leukemogenesis in adult mice by interacting with two other key regulators in LIC, Wnt/β-catenin and Bmi-1. 6, 7 It seems that SALL4 is a unique gene involved in self-renewal in embryonic stem cells and LIC. Therefore, we examined SALL4 expression in CML to determine whether it could be involved in the pathogenesis of this disease.