Our previous study demonstrated a positive feedback loop between RAGE and NF-κB during oxidative stress in pancreatic tumor cells exposed to chemotherapy.20 NF-κB activation within the tumor microenvironment regulates a number of genes important in cell death, metabolism, immunity, and inflammatory responses, contributing to oncogenesis.39 HIF1α is a master regulator of hypoxia15 and its expression and activity is also controlled by NF-κB.40,41 Here, we demonstrated that genetic and pharmacologic inhibition of NF-κB, but not HIF1α, significantly inhibits hypoxia-induced RAGE expression. The gene discussed is HIF1A; the disease is neoplasm.