The fact that we observed an expansion of the CD11b+/CD31-/Gr-1lo/Tie2+ population without an overall expansion of total CD11b+/CD31-/Gr-1lo monocytes in circulation when administering CSF1 to levels similar to that of breast cancer patients[15] suggests that CSF1 can actuate TEM differentiation from monocytes already in circulation which have potential to migrate to the tumor and become M1, tumor-fighting cells, yet are usurped by high serum levels of CSF1 to induce Tie2 receptor expression and adopt an M2-like, tumor supporting phenotype. This evidence concerns the gene TEK and breast cancer.