The observed increases in invasiveness and anchorage-independent growth of ErbB2-overexpressing SKBR3 cells following knockdown of IGFBP3 supports a role for IGFBP3 as a negative regulator of cellular transformation in breast cancer and we propose that its down-regulation is a mechanism whereby ErbB2 promotes tumour cell growth through increased IGF1-dependent proliferation, survival and invasion. This evidence concerns the gene IGF1 and breast carcinoma.