As MC-38 expresses high level of EGF and EGF is a predominant activator of ERK pathway in cancers [15,32,33], we investigated the function of EGF on regulating activation of ERK pathway and found blockage of EGF in MC-38 CM efficiently prevented the activation of ERK and inhibited the expression of CCL3, indicating CRC cells derived EGF at least partially activated ERK/CREB/CCL3 signaling in BMMs. This evidence concerns the gene CCL3 and cancer.