Recognizing that complex genetic differences among these cancer-derived cell lines are not limited to the HER2 and EGFR pathways, we then sought to evaluate how sensitivity to activation of AMPK correlates with EGFR activity in a syngeneic model using MCF10A cells, a non-tumorigenic human breast epithelial cell line, and derivatives of this cell line that were engineered by retroviral transduction to stably overexpress EGFR [19]. This evidence concerns the gene EGFR and cancer.