Previously, we proposed that HMGB1 can interact with LPS and transfer LPS to CD14 to enhance LPS-mediated inflammation [14]; HMGB1 may transfer LPS to CD14 under the conditions where LBP is absent, such as in LBP-deficient mice [19], or where and when the level of HMGB1 is highly increased such as in Gram-negative bacterial infections [9]. This evidence concerns the gene CD14 and gram-negative bacterial infections.