In the same year, Brouxhon et al. [36, 37] explored whether endogenous sE-cad levels (i) were overexpressed in HER2+ human and mouse BC specimens and tumors and cell culture systems of human triple-negative BC (TNBC), which does not express the genes for estrogen and progesterone receptors, and Her2/neu, and (ii) exerted prooncogenic effects via modulation of the HER-PI3K/Akt/mTOR-IAP axis and/or synergism with the HER ligand EGF. Here, MTOR is linked to breast cancer.