NFKB1 and neoplasm: The tumor immune microenvironment (TIME) molecular milieu supports chronic inflammation and associated carcinogenesis through immunosuppressive cytokines (TGF-β, IL-10, IL-4, IL-6, IL-13, and IL-33), reactive oxygen species (ROS), reactive nitrogen species (RNS), angiogenic factors [vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF-1α)], and carcinogenic inflammatory pathway stimulating transcription factors (TFs), including nuclear factor-kappa B (NF-κB) and signal transducer and activator of transcription-3 (STAT-3) [1–5].