The inhibition of a single receptor tyrosine kinase signaling presents a good example of molecular networks, which mediate tumor escape.2 A cross-talk of epidermal growth factor receptor (EGFR) and Met in transformed cells was already described in 2000 by Strom et al.3 EGFR is a member of the ErbB family of receptor tyrosine kinases consisting of EGFR (ErbB1), HER2/neu (ErbB2), HER3 (ErbB3) and HER4 (ErbB4).4 Constitutive EGFR signaling has a role in tumor biology by promoting survival and proliferation of cancer cells. This evidence concerns the gene MET and cancer.