In sepsis-induced liver injury, the LncRNA NEAT1 regulates the Let-7a/Toll-like receptor 4 (TLR4) axis to promote inflammation [8], while lncRNA MALAT1 deficiency attenuates interleukin-1β (IL-1β) and tumor necrosis factor-alpha (TNF-α) production during live injury [9], and lncRNA X inactivate-specific transcript (XIST) silencing ameliorates sepsis-induced acute liver injury by downregulating the expression of bromodomain-containing protein 4 (BRD4) [10]. This evidence concerns the gene TLR4 and injury.