Given the role of GSK-3beta in regulating dynamics of MT and in regulating junctional proteins, we examined whether GSK-3beta-dependent activation of GEF-H1/ROCK signaling promotes the disruption of beta-catenin and ZO-1 in lung vascular endothelial cell monolayers in vitro as well as increases lung vascular leak and ALI in vivo under septic conditions. This evidence concerns the gene ARHGEF2 and acute respiratory distress syndrome.