We previously reported that high expression levels of EGFR and low levels of constitutive EGFR activation were positively correlated with cetuximab sensitivity, which was determined via cell proliferation assays, whereas the activation of the RTK, MET, and mutations in KRAS or CDH1 were associated with cetuximab non-responsiveness using gastric cancer cell lines as a model system [6, 7]. Here, KRAS is linked to gastric cancer.