This massive recruitment of TAMs is usually facilitated by chemokines like CCL2, CCL5, VEGF, CSF-1, semaphorin 3A (SEMA3A), endothelin, eotaxin and oncostatin M. Once macrophages arrive in these tumour compartments, their migration is halted via hypoxia-dependent mechanisms. The gene discussed is SEMA3A; the disease is neoplasm.