CCL2 appears to hold the most potential due to its high expression in both the brain and blood at a basal state with evidence of alteration of the CCL2 and CCR2/MDSC axis in glioma and recent evidence supporting CCL2 and CCL7 inducing migration of MDSCs in the TME as well as association with a detriment in survival in GBM [81]. Here, CCL2 is linked to glioblastoma.