Although there are limited data available about the role of HMGB1 in neuroinflammation following sepsis, it has been implicated in other neurologic disorders, where its translocation from the nucleus to the extracellular space has been found to trigger neuroinflammatory reactions (such as regulating M1/M2 phenotypic polarization of microglia) and damage the blood–brain barrier. This evidence concerns the gene HMGB1 and Sepsis.