Treatments for metastatic breast cancer are palliative, lack specificity and often chemoresistance is developed to traditional treatments utilized. Therefore the identification of novel therapeutic targets critical to the metastatic cascade is important. One protein that has been shown to play vital roles in breast cancer cell migration and cell proliferation is growth factor receptor bound protein 7 (Grb7). This adaptor protein is commonly overexpressed with human epidermal growth factor receptor 2 (HER2) due to its close proximity to the HER2 amplicon. Grb7 functions by relaying signals between membrane bound receptors and downstream signaling cascades. This promotes focal adhesion kinase (FAK) signaling and receptor tyrosine kinase (RTK) signaling, promoting cell migration and cell proliferation respectively. Grb7 expression in a panel of breast cells ranging from highly epithelial (MCF10A) to highly mesenchymal (MDA-MB-231) was explored. Epithelial to mesenchymal transition (EMT) was also represented using MDA-MB-468 cells treated with increasing concentrations of epidermal growth factor (EGF). It was identified that Grb7 expression appeared to increase when EMT was stimulated. This was further explored by knocking down Grb7 using siRNA in the MDA-MB-468 cell line to determine if Grb7 is necessary for EMT. If Grb7 is necessary for EMT it is anticipated that peptide inhibitors of Grb7, developed in our laboratory, may act synergistically with other chemotherapeutic agents as a more targeted and effective treatment.