Furthermore, in vivo inhibition of SEMA7A and PLXNC1 by use of neutralizing antibodies in models of VILI and inhaled LPS models results in improved survival, reduced neutrophil migration and overall reduced cytokine response and lung injury (53, 101), suggesting their use a novel therapeutic agent for the management of ALI. The gene discussed is PLXNC1; the disease is acute respiratory distress syndrome.