Given that kinase-inactive EGFR is able to interact with and stabilize several cancer-relevant proteins [14], we speculated the redundant EGFR not bound to cetuximab in Caco-2 cells might further interact with MET in spite of kinase-inactivation by cetuximab inhibition, resulting in enhancement of the MET pathway and close associations between MET and SRC. Here, MET is linked to cancer.