This interpretation is supported by evidence of high SP-D levels in ARDS acute phase (as a result of a rupture of air-blood barrier) (49) and hyperproliferation of type II pneumocytes found in the proliferative phase of ARDS (occurring around 7 days after injury), which could lead to subsequent SP-D hyperproduction (50). The gene discussed is SFTPD; the disease is acute respiratory distress syndrome.