One of the known targets of its peptidase cleavage activity is CXCL12[30], and upregulation of DPP4 on the surface of CML LSCs may allow these cells to escape the homing/niche interactions imposed by the CXCL12/CXCR4 chemokine-receptor system[31], leading to dysregulated LSC growth and survival. This evidence concerns the gene CXCR4 and chronic myelogenous leukemia, BCR-ABL1 positive.