It is possible that in HMGB1–blocked mice subjected to APAP overdose, enhanced NF-κB activation diverts intracellular pathways from those associated with inflammation and cell death, to mechanisms linked to recruitment and activation of pro-regenerative programs, therefore, activation of NF-κB by blockade of HMGB1 might facilitate regeneration in this ALI induced by APAP. Here, HMGB1 is linked to acute respiratory distress syndrome.