Such explanations for this finding are: 1) ARDS pathophysiology in the infected subjects with moderate and severe illness is related to a massive loss of the angiotensin-converting enzyme (ACE)-2 enzyme, causing damage to the alveolar epithelium and vascular endothelium,41 2) compartmentalization of the inflammatory cascade, as described by Chow and Tisonciket al.,42,43 and 3) an acute phase response (APR) increase may be due to other pro-inflammatory cytokines, such as TNF-α or IL-1,31,39,40,44,45 and the aforementioned vicious cycle of cellular destruction. This evidence concerns the gene TNF and acute respiratory distress syndrome.