As in other at-risk populations, it is likely that multiple biological pathways drive the pathophysiology of ARDS after TBI.36–39 Recently, in a cohort study of 200 patients with severe TBI, Aisiku et al40 found an association between ARDS and an elevation in early inflammatory plasma cytokines, interleukin (IL)-6 and IL-8, and anti-inflammatory cytokine, IL-10. Our study builds on these findings by testing the association of a biomarker of vascular stability with ARDS after TBI. The gene discussed is IL10; the disease is acute respiratory distress syndrome.