Recent studies have shown that oncogenes like c-Myc, nuclear factor kappa B (NF-κB), tyrosine kinase receptors, and epidermal growth factors can turn on Ras/Raf or Akt-mediated pathways along with hypoxia-induced factor (HIF) to stimulate transcription of glycolytic genes to metabolically reprogram tumor cells (1–13). Here, NFKB1 is linked to neoplasm.