For instance, in triple negative breast cancer (TNBC), EGFR was suggested as a potential therapeutic target due to its overexpression in these cancers and promising anticancer activity of EGFR inhibitors some cell lines, but clinical trials with EGFR inhibitors failed to show clinically meaningful therapeutic effect, probably due to the existence of alternate compensatory signaling pathways6, 7. This evidence concerns the gene EGFR and triple-negative breast carcinoma.