One such mechanism may be similar to the one discussed previously in colon cancer, which suggests the role of MUC13 in augmented recruitment of cIAP1 to the TNFR/RIPK1 complex, and promotion of RIPK1 ubiquitination by cIAP1, which ultimately leads to NF-κB activation and downstream NF-κB-regulated gene expression [16]. The gene discussed is RIPK1; the disease is colonic neoplasm.