The use of G-PB DLI was based on the laboratory findings that G-CSF-priming could induce hypo-responsiveness of T cells for polarization from Th1 to Th2 and downregulation of the CD28/B7 pathway [10, 21] and augment NK-T cell dependent CD8+ cytotoxicity which might enhance GVL without GVHD [22]. The gene discussed is CSF3; the disease is graft versus host disease.