In view of the inverse association of HDL-cholesterol with several lung diseases as well as the protective effects of APOA1 overexpression or HDL mimetics in animal models of acute respiratory distress syndrome or pneumonia (18, 19), it will be very interesting to investigate the effects of HDL/SP-B interactions in bioassays that model pathogenic mechanisms in lung diseases. This evidence concerns the gene APOA1 and acute respiratory distress syndrome.