The tumor-promoting properties of AML are mediated mainly by angiogenesis, which stimulates endothelial cells to release chemokines (CXCL1, CXCL2) and growth factors (GM-CSF) to recruit neutrophils, and induces epithelial cells and fibroblasts to release monocyte chemoattractant protein 1 (MCP-1) to recruit monocytes to tumor sites to differentiate into TAMs [140], whereas TAMs lose their antitumor immune properties and are linked to unfavorable outcomes [141] (Figure 4). The gene discussed is CSF2; the disease is neoplasm.