In our preliminary data, investigators found PRMT can methylate EGFR, leading to up-regulation of EGFR signaling. The up-regulated EGFR signaling further triggered higher cell proliferation rate. In addition, cells with higher EGFR methylation level showed higher tumor growth ability in mice colorectal cancer xenograft model. Importantly, the cells with higher EGFR methylation level demonstrated higher cell growth rate in the presence of cetuximab in in vitro cell proliferation assay, suggesting that EGFR methylation may lead to resistance to cetuximab. In order to study the clinical correlation between EGFR methylation and cetuximab resistance, investigators propose to collect paraffin embedded tissue samples from patients with or without cetuximab treatment and analyze their EGFR methylation level. Investigators expect that patients with lower EGFR methylation level have higher improvement when treated with cetuximab compared to those without cetuximab treatment. In contrast, patients with higher EGFR methylation level showed poorer improvement when treated with cetuximab in comparison with patients without cetuximab treatment. By detecting EGFR methylation levels in these tissue samples and analyzing the correlation between EGFR methylation level and cetuximab response, investigators will provide an insight for prediction of cetuximab response in colorectal cancer therapy.