Within the TME, tumor cells are the source of chronic inflammation, and IL-1β becomes an upstream regulator, altering immunologic responses, hormonal signaling, neovascularization, and enhancing metastatic potential through downstream pathways such as NF-κB/MAPK/Protein Kinase B (AKT)/Wnt/β-catenin [13]. The gene discussed is NFKB1; the disease is neoplasm.