To establish whether inflammation is a potential mechanism contributing to the increased tumorigenesis in Ripk3−/− mice, we examined the expression of pro-inflammatory cytokines and chemokines in tumors and non-tumoral colonic tissues derived from WT and Ripk3−/− mice at day 91 after AOM-DSS, as these are key players in CRC. This evidence concerns the gene RIPK3 and colorectal carcinoma.