This includes tactics such as obstructing the CCL2-CCR2 axis to deter monocyte recruitment from the bone marrow to inflamed areas; impeding the CSF1-CSF1R axis to induce TAM apoptosis; or thwarting the CXCL12-CXCR4 and ANG2-TIE2 axes to remove distinct TIE2+macrophages vital for tumor angiogenesis [162, 169]. The gene discussed is CXCL12; the disease is neoplasm.