During cancer progression, increased VEGF165 expression can competitively block the binding of SEMA3B (and SEMA3A) to neuropilins, thereby enhancing breast cancer cell survival by maintaining a constitutive elevation in PI3K activity and angiogenesis, while SEMA3A and SEMA3B can competitively block the binding of VEGF165 to the neuropilins, inhibiting angiogenesis and metastasis [26]. This evidence concerns the gene SEMA3A and breast cancer.