After the activation of TLR, HMGB1 could acetylate and trigger its translocation from the nucleus to the circulation and interact with a variety of target cell receptors (RAGE, TLR2, TLR4, etc.), stimulating the release of pro-inflammatory cyto-/chemokines and leading to inflammations and sepsis (Yang et al., 2015; Abdulmahdi et al., 2017; Andersson et al., 2018). This evidence concerns the gene TLR4 and Sepsis.