Given that c-MET and EGFR signaling pathways share molecular nodes (PI3K/Akt, MAPK), and recent data show the possible compensatory function of these receptor tyrosine kinase stimulated pathways [25], we examined the in vivo effect of the c-MET inhibitor SU11274 on primary tumor growth and liver colonization ability of the cetuximab resistant PE/CA-PJ15 and the cetuximab sensitive PJ41 HNSCC cells. The gene discussed is EGFR; the disease is neoplasm.