Subsequent observations supporting a possible role of complement in ARDS, were reported in a prospective study of intensive care unit (ICU) patients who developed ARDS, revealing abnormal C3 consumption and elevated plasma C5a activity in the majority of ARDS cases [54], while another study provided evidence of C3 activation in plasma samples and C3 and C5a activation, in BALF samples of all patients with ARDS [55]. This evidence concerns the gene C5 and acute respiratory distress syndrome.