LAUSR

2035 with NAC at this point is insufficient to stop the progression of liver injury, in particular, because DAMP release may even precede the rise in plasma transaminases in some cases.(1) In addition to HMGB1, systemic concentrations of DAMPs such as double-stranded DNA and mitochondrial DNA are also raised after PCM overdose.(5,6) The inflammatory pathways activated by these DAMPs have been elaborately studied. Accordingly, blocking leukocyte DAMP receptors such as toll-like receptor 9 has shown promise in preclinical models of PCM toxicity.(7) The merits of neutralizing HMGB1 directly have also been demonstrated in animal studies.(8) Expanding the therapeutic repertoire for PCM overdose beyond NAC therefore seems an attainable objective for future research. To that end, the clinical validation of animal studies is highly needed.