Alterations resulting in enhanced epidermal growth factor receptor (EGFR) expression or function have been documented in a variety of tumors. Therefore, EGFR-tyrosine kinase is a promising therapeutic target. Althoughin vitro andin vivo studies have shown the anti-tumor activity of EGFR-tyrosine kinase inhibitors against various tumor types, little is known about the mechanism by which such inhibitors effect their anti-tumor action.