During infection or cellular stress, posttranslational modifications, such as JAK/STAT-mediated acetylation, phosphorylation and methylation, result in the relocation and accumulation of HMGB1 in the cytoplasm; however, because HMGB1 lacks a leader peptide sequence, it is not actively secreted via the endoplasmic reticulum/Golgi exocytotic pathway. This evidence concerns the gene HMGB1 and infection.