Equally important, the critical limitation of pleiotropic neutrophil inhibitors in the context of ongoing infections and risk for secondary infections as in ARDS and COVID-19-ARDS, the target-specific inhibition of DEspR+ rogue neutrophils will spare DEspR[-]CD11b+ activated neutrophil subsets, hence preserve neutrophil defense functions against infections pertinent to critically ill patients with ARDS or COVID-19-ARDS. This evidence concerns the gene ITGAM and COVID-19.