For this purpose several strategies have been developed, including; hampering the monocyte infiltration and macrophage differentiation in the tumor sites (e.g., CCL2 or CSF-1 blocking antibodies), deletion of M2 macrophages in the TME (e.g., antibodies against CD206, scavenger receptors or other M2-associated molecules), or repolarization toward the M1 phenotype and enhancement of their anti-tumor properties (e.g., delivery of activating stimuli and/or antibodies inducing macrophage' phagocytosis, or ex vivo macrophage manipulation) (75–77) (Figure 1). Here, MRC1 is linked to neoplasm.