KRAS mutation, which is typically associated with tumor progression and poor prognosis, was reported to occur in 35–50% of CRC patients.5,6 The roles of KRAS in CRC pathogenesis were faithfully indicated by genetically engineered CRC mouse models, in which the conditional expression of the mutant allele of KRAS promoted tumor invasion and metastases.7 Moreover, mutationally activated KRAS was found to elicit intrinsic resistance to epidermal growth factor receptor inhibitors.8 These insights imply that KRAS exerts complex effects in tumors. This evidence concerns the gene EGFR and neoplasm.