Several studies demonstrated that acquired resistance to drugs that block ER signalling is the consequence of activation of alternative survival signalling via growth factor receptors, such as epidermal growth factor receptor (EGFR) and human epidermal growth factor 2 (HER2), that enable ERα + ve breast cancer cells to escape anti-estrogen actions and contribute to an invasive phenotype [5,6]. This evidence concerns the gene ESR1 and breast carcinoma.