It has been proposed that tumour cells may escape the inhibitory effects of antioestrogens by increasing ligand-independent phosphorylation of ER, possibly as a result of an overexpression of growth factors, namely the EGFR, Her-2/neu (HER2) and the IGF-IR pathways through increased levels of mitogen-activated protein kinases (MAPKs) (Chen et al, 2002; Lannigan, 2003). This evidence concerns the gene EGFR and neoplasm.