It has been proposed that the increased susceptibility of IL-18 deficient mice to colitis and cancer in the AOM/DSS model may be partially dependent on MyD88-related mechanisms, although Il-18 deficient mice present a milder phenotype compared with Myd88 knockout mice (less tumorigenesis) implying that other MyD88-related pathways might act with IL-18 to minimize carcinogenesis [8]. This evidence concerns the gene MYD88 and colitis.