Links between the EGFR-dependent processes and mammary gland pathophysiology are further reinforced by the observations that EGFR is either amplified or overexpressed in a considerable proportion of basal-like breast cancers [16,17]; transcripts for EGFR ligands such as epidermal growth factor (EGF), AREG and transforming growth factor alpha (TGFα) are frequently upregulated in human breast cancer samples and a majority of breast cancers that express high levels of TGFα also co-express EGFR, suggesting a potential autocrine loop [18–22]. This evidence concerns the gene AREG and breast carcinoma.