Indeed, this principle has been demonstrated in breast cancer in a recent study that used an EGFR/HER2/VEGFR multi-RTK inhibitor (AEE788) in combination with mTOR rapalogs (rapamycin, temsirolimus, or everolimus) to re-sensitize triple-negative breast cancer cells to mTOR-targeted inhibition [202]. This evidence concerns the gene ERBB2 and triple-negative breast carcinoma.