Altered tumors are characterized by the activation of tumor-cell-intrinsic oncogene pathways such as Wnt/β-catenin and nuclear factor kappa-B (NF-κB); presence of tumor-soluble inhibitory mediators such as vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β); increased levels of immunosuppressive cells such as myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and tumor-associated macrophages (TAMs); epigenetic changes in the TME; and metabolic competition (hypoxia, overconsumption of glucose, etc.)(Galon and Bruni, 2019). The gene discussed is NFKB1; the disease is neoplasm.