HMGB1 can enter endosomal vesicles for eventual secretion after immune activation or other type of stimulus.When cells die by necrosis or apoptosis, HMGB1 also translocates to the extracellular milieu [3, 12], and its immunological effect is different.When HMGB1 is liberated by necrotic cells induces strong pro-inflammatory stimulus, as demonstrated in models of sepsis [13], while HMGB1 released during apoptosis could diminish immunological activity, due to the oxidation of key cysteine residues occurring during redox disturbances in stressed cells [14]. Here, HMGB1 is linked to Sepsis.