We tested this hypothesis in basal-like breast cancer (BLBC) cells, because of previous studies on Cdc42 and c-Cbl interactions in such cells (Hirsch et al, 2006) and also because of the importance of developing improved treatments for these aggressive cancers that are resistant to the front-line breast cancer treatments of Herceptin® (Trastuzumab), TMX and aromatase inhibitors. This evidence concerns the gene CYP19A1 and breast carcinoma.