Stem cell mobilization with potent G-CSF analogs activates iNKT cells with subsequent promotion of donor CTL function and GVL effects. After stem cell mobilization with potent G-CSF analogs, donor iNKT cells are expanded and functionally activated. These iNKT cells interact with residual host APCs and may be activated directly through CD1d-presented glycolipid or indirectly through cytokines (including IL-12 and IL-18). After activation, iNKT cells secrete large amounts of cytokine, including IFN-γ, which further primes host APCs and activates cellular effectors of the innate (NK cell) and adaptive (CD4⁺ and CD8⁺ T cell) immune systems. NK cells are activated by host APCs through activating receptor interactions (including NKG2D-NKG2Dl and CD70-CD27) and cytokines (including IFN-α/β, IL-12, IL-15, and IL-18). NK cells reciprocally enhance APC activation through the secretion of IFN-γ and TNF-α and directly mediate MHC-independent GVL through interactions with activating ligands, KIR mismatch, or the recognition of leukemic targets lacking MHC class 1. Donor CD4⁺ T cells, activated by host hemopoietic or leukemia-specific antigens presented by host (or donor) APCs, mediate GVL effects against MHC class 2⁺ leukemic targets expressing the relevant antigens. Donor CD8⁺ T cells activated by a similar range of antigens, presented by host APCs only, mediate GVL against leukemic targets expressing the relevant antigens within MHC class 1.