More importantly, the convergence of our ex vivo data with cumulative reports implicating neutrophils, along with the potential for targeted inhibition of DEspR+CD11b+ neutrophils shown in patient samples ex vivo with ARDS (12) and preclinical efficacy of DEspR-inhibition observed in a spontaneous ICH rat model (14), altogether provide the basis to further test DEspR+CD11b+ neutrophils and NET-forming neutrophils as a potential actionable neutrophil-specific therapeutic target in sICH. This evidence concerns the gene ITGAM and acute respiratory distress syndrome.