The possible reason was that upregulated lnc‐THRIL might induce the release of TNF‐α as well as the subsequent boost of inflammatory mediators, which might elevate the level of radicals in lung microcirculation to injure the alveolar epithelial cells, thereby disrupted the barrier of lung microcirculation and subsequently increased the risk of ARDS in sepsis patients.12 This evidence concerns the gene TNF and acute respiratory distress syndrome.