Although TIMP-3 has not been studied in ARDS, it plays an important role in the mouse models of postinjury brain edema, and its role in vascular leak and localization in the lung tissue supports the biological plausibility for a role in ARDS.18 20 The association between TIMP-3 and poor clinical outcomes after isolated TBI is consistent with the hypothesis that dysregulated MMP activity may be involved in vascular endothelial stability and play an important role in the pathogenesis of complications after injury, such as ARDS and death, in patients with TBI. The gene discussed is TIMP3; the disease is acute respiratory distress syndrome.