We have recently shown that in vivo deficiency of ITSN-1s, an isoform of ITSN-1 that is highly prevalent in lung endothelium and deficiency of which is relevant to the pathology of ALI/ARDS (Bardita et al., 2013; Predescu et al., 2013), induces extensive lung endothelial cell apoptosis and injury; after only 7 days of ITSN knockdown (KD-ITSN), the remaining endothelial cells exhibited phenotypic changes including hyperproliferation and apoptosis resistance against ITSN-1s deficiency, leading to increased microvessel density, repair and remodeling of the injured lung. Here, ITSN1 is linked to acute respiratory distress syndrome.