Since we demonstrated that DA-3 mammary tumor cells produce SEMA7A, and that treatment of macrophages with rmSEMA7A induced the production of proangiogenic CXCL2/MIP-2, we hypothesized that silencing SEMA7A gene in DA-3 mammary tumor cells would have an inhibitory effect on production of CXCL2/MIP-2 by macrophages treated with tumor cell supernatants silenced for the SEMA7A gene. The gene discussed is CXCL2; the disease is breast cancer.