Since anti-DEspR hu6g8 has been shown to bind, internalize, translocate to the nucleus over time, and induce apoptosis in macaque DEspR+ neutrophils as observed in prior ex vivo studies (23), as well as in pancreatic cancer cells (31), in vivo efficacy of anti-DEspR in transient LPS-ALI and high-mortality LPS-encephalopathy models in this study provide further proof-of-concept data that induction of neutrophil apoptosis is the therapeutic path to attaining neutrophil function shutdown, efferocytosis and active resolution of inflammation (35–37). This evidence concerns the gene FBXW7-AS1 and acute respiratory distress syndrome.