Re-programming of macrophages from an immune-inhibitory M2-like subtype toward an immune-stimulatory M1-like subtype, by targeting the VEGF receptor 2, enhanced anticancer efficacy in a CD8+ T-cell–dependent manner in murine breast cancer models, suggesting that combination of anti-angiogenic therapy with other types of drugs may facilitate anti-tumor effects by altering the phenotype of TAMs (76). This evidence concerns the gene CD8A and neoplasm.