These results are consistent with previous findings showing that the BM CD11b+Gr1+ myeloid cell compartment expands in response to tumor-derived G-CSF and is functionally altered before these cells are mobilized into the circulation (54, 55), via the activation of the retinoic-acid-related orphan receptor (RORC1/RORγ) and CCAAT/enhancer-binding protein β (C/EBPβ) pathways (56). This evidence concerns the gene ITGAM and neoplasm.