Our findings imply that ACE2 may be applied to improve LPS–induced lung injury via regulation of the ACE2/ACE/AngII/Ang–(1–7)/Mas receptor, by inhibiting the JNK/NF–kB signaling pathway and that upregulation of the ACE2/Ang–(1–7)/Mas axis and inhibition of JNK/NF–kB activation may be an effective therapeutic strategy against ARDS in clinic. This evidence concerns the gene ANG and acute respiratory distress syndrome.