There are a number of possible explanations for the protective effect of GLN against ALI during sepsis, including enhanced expression of heat shock protein (HSP), activation of peroxisome proliferator-activated receptor (PPAR)-γ, buffering of oxidative stress, inhibition of HMGB-1 expression, and anti-inflammatory responses [13, 15]. The gene discussed is HMGB1; the disease is acute respiratory distress syndrome.