In the transcriptome study (GEO dataset GSE57011), SEMA3A was identified as the most downregulated gene in ARDS patients [20], and overexpression of SEMA3A in the lipopolysaccharides (LPS)-induced ARDS model alleviates oxidative stress and inflammation by suppressing activation of the extracellular signal-regulated kinase/Jun-N-Terminal Kinase (ERK/JNK) signaling pathway in rat pulmonary microvascular endothelial cells [20]. This evidence concerns the gene MAPK8 and acute respiratory distress syndrome.