Lastly, our current mechanistic and therapeutic studies in diverse small and large preclinical models, indicate that circulating eNAMPT directly contributes to the pathobiology of ARDS/VILI via upstream TLR4 activation, a key innate immunity inflammatory cascade driving NFkB transcriptional activities and loss of lung vascular barrier integrity9–11. The gene discussed is NFKB1; the disease is acute respiratory distress syndrome.