Although epithelial-specific deletion of IFNAR1 did not impact on the severity of spontaneous or DSS-induced intestinal inflammation, they exhibited increased tumor burden in the azoxymethane/DSS model of colitis-associated colon cancer (76), Both spontaneous epithelial hyperproliferation and tumor promotion are dependent on the microbial flora, since differences between wild-type and IEC-specific IFNAR1-deficient mice were only apparent if the mice were housed separately (76). This evidence concerns the gene IFNAR1 and colonic neoplasm.