Previous studies also demonstrated the dual regulation between NF-κB and HIF-1 in cellular cultures (82, 83) Hypoxia also potentiates the NF-κB signaling by modulating the expression of toll like receptors (TLRs), which are known for their functional roles in the inflammatory response in both, infectious and non-infectious diseases and in the production of IL-1β, a main pro-inflammatory cytokine (55, 84). This evidence concerns the gene NFKB1 and infectious disease.