The results indicated that SOCS-1, as a downstream target, could be regulated by lncRNA MALAT1 in smoke inhalation-induced ALI, which would also explain the crucial role of MALAT1 in HA1600 alleviated lung damage, while whether MALAT1 suppresses NALP3 inflammasome formation and even the DISC apoptosis pathway deserves to be further investigated. This evidence concerns the gene MALAT1 and acute respiratory distress syndrome.