Interestingly, a bivalent antibody specific to both IL1PRAP and CD176 was found to target the cell population of CML but not their corresponding normal cells.56 Another study demonstrated that BCR-ABL CML CD34+/CD38-/CD26+LSC cells are resistant to TKI.57 Interestingly, it turned out that the pathways of TGF-ß and TNF-α were dysregulated in both BCR-ABL- and BCR-ABL+ CML-LSC with increased LSC quiescence and resistance to TKI. This evidence concerns the gene DPP4 and chronic myelogenous leukemia, BCR-ABL1 positive.