In Sef knockout mice induced to develop colitis-associated colorectal cancer, the Sef loss stimulates colon tumorigenesis by promoting the activation of TLR and IL-17 signaling, which enhances STAT3 tyrosine phosphorylation, thus leading to the expression of pro-inflammatory cytokines, including IL-17A and IL-6. Here, IL17RD is linked to colorectal cancer.