To test whether unpalmitoylated EGFR is the main mechanism that increases TKI sensitization in breast cancer, we expressed a tetracycline-inducible palmitoylation-defective EGFR (EGFRC1025A) in MDA-MB-231 cells that led to increased cell death after gefitinib treatment compared to those expressing inducible wild-type EGFR, suggesting that the sensitization of triple-negative breast cancer cells to gefitinib is mediated by unpalmitoylated EGFR [48,54]. This evidence concerns the gene EGFR and triple-negative breast carcinoma.