Although it is not clear whether the attenuation observed in this model was caused by inhibition of HMGB1 release from macrophages or direct inhibition of the p38 MAPK and NF-kB signaling pathways, these results suggest that, in addition to inhibiting lethal sepsis in an in vivo model, anti-HMGB1 treatment might inhibit ALI and suppress subsequent fibrosis. The gene discussed is NFKB1; the disease is Sepsis.