NOD1 deficiency alone or together with a mutation in Apc (ApcMin/+) leads to increased risk of tumor formation in the AOM/DSS mouse model of colon cancer. Increased tumor formation is a consequence of increased intestinal epithelial apoptosis as well as intestinal permeability associated with enhanced inflammatory cytokine production and epithelial cell proliferation. This evidence concerns the gene APC and colonic neoplasm.