The demonstrations of efficacy of DEspR inhibition in vivo in two independent animal LPS-inflammatory models in reducing neutrophil-induced secondary tissue injury damage, 1) hypoxemia in macaques and 2) brain edema and encephalopathy in hypertensive rats, together indicate a pathophysiological role of the DEspR+ rogue neutrophil subset. This evidence concerns the gene FBXW7-AS1 and Encephalopathy.