While the β-AR could serve as a therapeutic target to increase the proportion of TCR-γδ T-cells in peripheral blood stem cell grafts (e.g., by administering a β-AR agonist to G-CSF mobilized donors), it is not known if systemic β-AR activation will alter the responsiveness of TCR-γδ T-cells to ZOL+IL-2 ex vivo or alter the ability of the expanded cells to recognize and kill tumor targets. This evidence concerns the gene CSF3 and neoplasm.