In line with observations in C57BL/6 mice, A-HDL treatment enhanced ALI/ARDS phenotypes in apoA-I KO mice after CLP including alveolar histopathologic changes, lung permeability, lung edema and alveolar inflammation (Fig. 3b–f), while A-HDL and N-HDL treated mice showed the comparable levels of plasma LPS in these mice (Fig. 3g). The gene discussed is APOA1; the disease is acute respiratory distress syndrome.