SIGIRR, also named Toll-like receptor/interleukin-1 receptor 8 (TIR8), and a member of the TLR-IL-1R receptor superfamily were involved in the pathological process of ALI by regulating the NF-κB activation to release the cytokines and chemokines, and increased SIGIRR expression could inhibit LPS-induced ALI by downregulating the LPS-TLR-4 pathway [17, 18]. Here, TLR4 is linked to acute respiratory distress syndrome.