This idea is supported by our observation that BCR-ABL causes an increase in the LSC population and that the defect in CML induction by BCR-ABL in the absence of Alox5 is associated with increases in Icsbp expression and the percentage of BCR-ABL-expressing apoptotic LSK− cells (Fig. 6F). This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.