Further, genome-wide transcriptomics have also provided insight into the mechanisms of distinction between CP and BC, progression and resistance of CML on the whole blood of different phases of CML-patients, cell lines, leukemia stem cells, and normal stem and progenitor cell populations [6, 10, 17] Radich et al. [6] showed an association of decreased expression of Jun B and Fos with other deregulated pathways with early accelerated phase and identified 6 genes (NOB1, DDX47, IGSF2, LTB4R, SCARB1, and SLC25A3) that discriminated CP from BC [6]. This evidence concerns the gene CD101 and breast cancer.