Support for this includes (i) reduced systemic cytokine production including IL-1β in 5-LOX−/− mice in a cecal ligation and puncture (CLP)-induced peritonitis model (Monteiro et al., 2014), (ii) S100A8/A9 sequestration by arachidonic acid that possibly becomes accumulated due to a lack of active 5-LO (Kannan, 2003), or (iii) downregulation of S100A8 expression in 5-LOX−/− mice in the absence of LTA4 which was shown to scavenge S100A8/A9 proteins for protection from hydrolytic degradation (Rector and Murphy, 2009). The gene discussed is ALOX5; the disease is peritonitis.