RosA effectively inhibited the release of HMGB1 in human endothelial cells and downregulated HMGB1-dependent inflammatory responses; RosA supressed HMGB1-mediated high permeability and leukocyte migration in mice; RosA decreased CLP-stimulated HMGB1 release and sepsis-related mortality. The article suggested that RosA ought to be considered as a candidate therapeutic for treating all kinds of inflammatory diseases by inhibiting the HMGB1 pathway. RosA was a potential treatment for curing serious vascular inflammatory diseases like sepsis and septic shock. The gene discussed is HMGB1; the disease is Sepsis.