Asano et al. used human brain tumor cells with different CCL2 expression levels (native HBT28: high CCL2; HBT20: low CCL2 and CCL2-transfected HBT28 and HBT20 cells) and showed that the propensity of LPS-activated human monocytes to inhibit tumor cell growth was dependent on the basal CCL2 expression level of the tumor cells (94). Here, CCL2 is linked to brain neoplasm.