Finally, through administration of the Shp1-activating small molecule SC43 (27, 28), we inhibited agonist-induced neutrophil ROS production in vitro and reduced alveolar neutrophilia and NETs in vivo, conceptually supporting Shp1 activation as a therapeutic approach to fine tune neutrophil function in ARDS. The gene discussed is PTPN6; the disease is acute respiratory distress syndrome.