In a bacterial lipopolysaccharide (LPS)-induced sepsis mouse model, pulmonary endothelial heparanase was activated in a TNF-α dependent manner.12 Consequently, the increase in heparanase activity leads to the development of acute lung injury during endotoxemia.12 In that study, the authors also demonstrate the enhanced diffuse alveolar damage by heparanase from biopsied human lung tissue. Here, HPSE is linked to Sepsis.