The inhibitory effect of knockdown of MALAT1 on lung injury has been reported in several studies; for instance, silencing of MALAT1 could regulate the progression of acute lung injury through NF-κB and p38 MAPK pathways, and could also inhibit inflammation by upregulating miR-146a in lipopolysaccharide-induced acute lung injury.34, 35 Besides, upregulation of IL-8 could induce negative graft function, as well as increase mortality after lung transplantation, whereas inhibition of IL-8 by administration of mesenchymal stem cells (MSCs) improves the graft function after transplantation.36 The gene discussed is MALAT1; the disease is injury.