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]. This evidence concerns the gene HSP90B2P and acute respiratory distress syndrome.