MCL1 and chronic myelogenous leukemia, BCR-ABL1 positive: Therefore, the eradication of LSCs may be a hopeful strategy for radical treatment of CML.[7] Currently, several pathways or regulators that uniquely maintain LSCs have been identified, including B‐cell lymphoma 2 (Bcl‐2) and myeloid cell leukemia 1 (Mcl‐1), Wnt/β‐catenin and Hedgehog pathways, arachidonate 5‐lipoxygenase (Alox5) and stearoyl– coenzyme A desaturase 1 (Scd1), p53 and c‐Myc network, and the hematopoietic microenvironment.[8, 9] However, the precise regulation of LSCs self‐renewal remains incompletely characterized.