This could be explained in part by the finding that pro-inflammatory cytokines such as IFN-γ and TNF-α, and agonists of Toll-like receptors (TLRs) upregulated the expression of CYP27B1 in monocytes, macrophages, and dendritic cells139,140 suggesting that the pro-inflammatory tumor microenvironment could be a contributing factor for increased CYP27B1 expression in immune cells, which is opposite to the finding in colon cancer cells133 mentioned above. This evidence concerns the gene CYP27B1 and colonic neoplasm.