By now there is considerable evidence supporting the role of estrogen as a mediator in the production of proinflammatory cytokines, namely IL-1, IL-6 and TNF-α20 and at least there are plausible explanations for differences in development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) where different pathways have been described, resulting in less barrier dysfunction and inflammation in female rat lungs19. The gene discussed is IL6; the disease is acute respiratory distress syndrome.