Thus, considering the biological mechanism by which HO-1 induction attenuates brain dysfunction during experimental cerebral malaria, we can speculate that during experimental MA-ALI, the induction of HO-1 downmodulates CD8+ T cell activation and migration to lung tissue, reduces the production of inflammatory mediators, and restores endothelial cell barrier integrity. This evidence concerns the gene HMOX1 and acute respiratory distress syndrome.