In this model, most mutations, including APC and KRAS, occur less often than in sporadic CRC and at later stages of tumor evolution, where they promote cytokine secretion, tumor growth, and angiogenesis via the NF-κB, IL-6/STAT3, or IL-23/Th17 pathways [29,30,31]. The gene discussed is NFKB1; the disease is neoplasm.