From the extensive analysis of many breast tumors it is well established that ErbB tyrosine kinase receptors, in particular ErbB2 and ErbB1 (epidermal growth factor receptor, EGFR), often become constitutively active in breast cancer as a result of overexpression, or in the case of ErbB1, autocrine ligand production or mutation (for reviews see [1-4]). This evidence concerns the gene NTRK1 and breast carcinoma.