In a mouse model of inflammation-induced colorectal cancer, the administration of antibodies blocking the interaction of DCIR with asialo-biantennary N-glycans reduced tumor incidence by reverting the DCIR-dependent blockade of alarmin recognition by TLRs, suggesting a crucial role for DCIR in the maintenance of the intestinal immune system functionality and that DCIR may represent a promising target for the treatment of colitis and colon cancers (161). This evidence concerns the gene CLEC4A and colorectal cancer.