RIPK3-deficient mice exhibited high activation of NF-κB in dysplastic and non-dysplastic areas of the colon evidenced by dramatic increase in the expression of IL-6, an iconic cytokine induced by NF-κB and responsible for CRC progression through IL-6-induced STAT3 signaling [35, 37]. This evidence concerns the gene RIPK3 and colorectal carcinoma.