Recently, Bopp et al. demonstrated that sRAGE concentrations in sepsis patients were higher in non-survivors when compared with survivors. They concluded that larger clinical trials should study the potential role of sRAGE as a new sepsis marker [37] . However, sRAGE has been used in animal models to block HMGB-1's binding to the RAGE receptor, leading to increased survival. This data indicates that HMGB-1 and RAGE participate in sepsis, including sepsis patients with CAP.