Using bone marrow (BM) chimeric mice to construct AOM/DSS-induced CAC model, Fukata et al. [24] reported that the infiltration of neutrophils and macrophages as well as the expression of chemokines CCL2 and keratinocyte-derived chemokine were higher in WT mice engrafted with TLR4−/− BM than in TLR4−/− mice engrafted with WT BM, indicating that TLR4 signaling on colonic epithelial cells rather than the myeloid compartment could promote the recruitment of inflammatory cells in the tumor microenvironment of CAC. This evidence concerns the gene TLR4 and neoplasm.