Most macrophage-targeting therapies have three goals (9, 64): (1) inhibit macrophage recruitment by blocking the C-C motif chemokine ligand 2 (CCL2)/C-C motif chemokine receptor 2 (CCR2) axis (65, 66); (2) deplete macrophages or block -factor (CSF)-1/CSF-1R signaling (67, 68); (3) reprogram TAMs toward an M1-like phenotype using melittin (69), IFN-γ (70), CD40 agonists (71), or tumor hypoxia-targeting agents (72). The gene discussed is CCL2; the disease is neoplasm.