It is well-known that anti-VEGF therapy can cause tumor hypoxia due to excessive vessel regression, M2-TAMs attracted by oncostatin M and eotaxin from hypoxic tumor cells might be a compensatory mechanism to secure tumor angiogenesis through providing pro-angiogenic factors (47), which seems partially responsible for the resistance to anti-VEGF therapy. The gene discussed is CCL11; the disease is neoplasm.