DPP4 targets CXCL12 with its peptidase cleavage activity, and its upregulation may favor a dysregulated growth and survival of CML-LSCs through the escape of the homing/niche interactions imposed by the CXCL12/CXCR4 chemokine-receptor system (26, 27). This evidence concerns the gene CXCR4 and chronic myelogenous leukemia, BCR-ABL1 positive.