Additionally, our previous research also indicated that lidocaine could induce the upregulation of SOCS3, and using SOCS3 small interfering RNA to knockdown SOCS3 sufficiently abolished anti-inflammatory effects of lidocaine; besides, we also found that lidocaine induced upregulation of SOCS3 expression in an AMPK-dependent manner [17], and recent studies have also attempted to use the anti-inflammatory cytokines, such as IL-4, IL-10, and IL-13, to inhibit TF expression in monocytes and protect against ALI [47]. Here, IL4 is linked to acute respiratory distress syndrome.