The use of a large number of genetically defective mice (e.g., activating transcription factor 3 [ATF3]−/−183, C-C motif chemokine receptor 7 [CCR7]−/−184, IL17A−/−185, secretory leukocyte peptidase inhibitor [SLPI]−/−186, complement C3 [C3]−/−187, and ADAM metallopeptidase with thrombospondin type 1 motif 13 [ADAMTS13]−/− mice188) in infection models further confirms the complexity and diversity of the HMGB1 release mechanism. This evidence concerns the gene ATF3 and infection.