Importantly, these processes could be dramatically inhibited by a treatment of anti-ADAM28 antibody or small interfering RNA to ADAM28, suggesting that ADAM28 had a clinical implication in breast cancer cell proliferation through enhanced bioavailability of IGF-I released from the IGF-I/IGFBP-3 complex by selective IGFBP-3 cleavage [20]. This evidence concerns the gene IGF1 and breast carcinoma.