Interestingly, serum from MCD mouse group that showed NASH pathophysiology and containing high circulatory Lcn2-induced HMGB1 secretion in brain endothelial cells in 24 h while it was significantly decreased in 24p3RsiRNA-treated brain endothelial cells suggesting a clear role of Lcn2 in HMGB1 release though other mediators may not be ruled out. This evidence concerns the gene HMGB1 and metabolic dysfunction-associated steatohepatitis.