EGFR and breast carcinoma: This result could be explained by the possible role of D609 as a stress-inducer able to elicit ligand-independent EGFR internalization [51], thus reducing the constitutive expression of the receptor and, likely, to stimulate its degradation, as already reported by Cichocki and colleagues in HaCaT cells [52] and by our group in breast carcinoma [25].