Together, these models highlight how dysregulation of specific signaling pathways--including PPARD-mediated metabolic reprogramming, gp130/STAT3-driven inflammatory signaling, TGF-β/Smad3 tumor suppressor loss, NF-κB1 knockout-induced cytokine dysregulation and immune cell infiltration, innate immune signaling disruption through MyD88, and hyperactivation of the Wnt signaling pathway--can individually or synergistically drive the development and progression of gastric cancer in vivo. This evidence concerns the gene NFKB1 and neoplasm.