To test the role of the thioredoxin system in the regulation of the HMGB1 redox status in the extracellular space, we specifically inhibited the TrxR activity in monocytes from HD pre-treated with PGE2. Indeed, the TrxR inhibitor Auranofin led to a fast oxidation of HMGB1, similarly to what observed in the supernatant of untreated monocytes, proving the relevance of the thioredoxin system in the modulation of the redox status of HMGB1. The gene discussed is TXN; the disease is Huntington disease.