The pathophysiology of ARDS is complex; in the early phase, mechanisms for pulmonary edema formation include dysfunction of the alveolar–capillary barrier, recruitment of polymorphonuclears and an increased amount of cytokines in plasma and bronchoalveolar lavage fluid, mainly Interleukin-1β (IL-1β), Interleukin-6 (IL-6), Interleukin-8 (IL-8) and Tumor Necrosis Factor-α (TNFα) [4]. This evidence concerns the gene IL1B and acute respiratory distress syndrome.