The inflammatory response through the HIF-1α signaling pathway is mainly due to IL-6/STAT3 axis and NF-κB. Studies indicated that the axis NF-κB2/p100 [23] or the phosphorylated NF-κB [24, 25] and the NF-κBp65/RelB heterodimers [26] played pivotal roles in endotoxin tolerance during sepsis in human monocytes. This evidence concerns the gene RELB and Sepsis.