Therefore, we postulate that tumor-derived fractalkine release stimulates mobilization of CD11b+CX3CR1+ monocytes through fractalkine/CX3CR1 interaction, and these mobilized CD11b+CX3CR1+ monocytes in the PB have angiogenic and/or immunosuppressive activity in the tumor microenvironment. This evidence concerns the gene CX3CR1 and neoplasm.