Thus, blocking the interaction of the cortactin SH3 domain with AMAP1 (a GTP-Arf6 effector overexpressed in invasive mammary tumours) with a cell-permeable peptide derived from the AMAP1 sequence, or a small-molecule compound, was found to effectively inhibit AMAP1/cortactin binding, and breast cancer invasion and metastasis (Hashimoto et al, 2006). This evidence concerns the gene CTTN and breast cancer.