To elucidate potential mechanisms underlying treatment responses to EGFR-targeted therapy, we here comprehensively investigated 7 CRC cell lines and tissue specimens of 25 CRC patients for putative resistance mechanisms residing within the target (i.e. EGFR), mutations of downstream signaling pathways or in bypass receptor tyrosine kinases as well as E-cadherin expression. The gene discussed is EGFR; the disease is colorectal carcinoma.