The existing bidirectional feedback between EGFR signaling and estrogenic activity is essential for the preservation of malignant phenotype in the breast cancer cells; since both pathways converge in the transactivation of genes correlated with the tumor proliferation, survival, aggressiveness; such as MYC [69, 70], B cell lymphoma 2-like protein (Bcl-XL) [71, 72], cyclin D1 (CCND1) [73, 74], cyclin-dependent kinase inhibitor A1 (CDKN1A) [75, 76] and the subunits that integrate the activator protein 1 (AP1) [77, 78]. This evidence concerns the gene MYC and breast carcinoma.