Because the pathogenesis of ALI/ARDS is complex, involving the abnormal activation of various immune cells such as dendritic cells, NK cells, macrophages, and neutrophils, gut microbiota dysbiosis, and the cross-regulation of multiple inflammatory signaling pathways such as mTOR, NF-κB, TLR, and JAK-STAT, and is often accompanied by cytokine storms, single-target therapy often has limited efficacy [28]. This evidence concerns the gene SOAT1 and acute respiratory distress syndrome.