It has also been suggested that MET is required for epithelial growth factor (EGF)-induced cell invasion and motility in EGFR wild-type NSCLC cells, especially as the pharmacological inhibition of c-Met or its siRNA knockdown reduced EGF-induced invasion and motility, indicating that EGFR requires c-Met activity and/or expression to maximize the invasive phenotypes of NSCLC cells [10]. Here, EGF is linked to non-small cell lung carcinoma.