Other treatment approaches targeting TAMs include reprogramming M2 macrophages to M1 (e.g., using low doses of radiation, targeting toll-like receptors, or use of zoledronic acid) or depleting existing M2 macrophages (e.g., by targeting the CSF-1/CSF-1R pathway), which cause resistance to cancer therapies, preventing TAM recruitment to tumor tissue (e.g., using anti-CCL2 antibodies or CCR2 inhibitors), and preventing TAM-mediated angiogenesis (via anti-VEGF antibody) [15]. Here, CCR2 is linked to neoplasm.