In CML, Bcr-Abl up-regulates TGF-β 1 expression, and released TGF-β 1 activates a PI3K/Akt/NF-κB/MMP9 signaling pathway from the stroma that subsequently results in the release of s-KitL and s-ICAM-1 (InterCellular Adhesion Molecule 1), ultimately enhancing the recruitment and mobilization of tumor stem cells to the peripheral circulation [97]. The gene discussed is ICAM1; the disease is neoplasm.