Here, we studied (1) whether DEspR+ neutrophils comprise a neutrophil-subset associated with ARDS and COVID-19-ARDS severity or mortality, (2) whether identification of the DEspR+ neutrophil-subset is reproducible in different research labs and concordant with scRNA-seq findings in severe COVID-19, and (3) whether DEspR+ neutrophils can be safely inhibited as a potential therapeutic target on dysregulated neutrophils. This evidence concerns the gene FBXW7-AS1 and acute respiratory distress syndrome.