In addition, salt-inducible kinase 2-mediated HDAC4 phosphorylation in LPS-activated macrophages was inhibited by Escitalopram, a drug used to treat depression, and the HDAC4 phosphorylation level was reduced and shifted to the nucleus, promoting p65 deacetylation and cytoplasmic shuttling and attenuating NF-κB inflammatory pathway activation, thereby improving sepsis-associated ALI [143]. This evidence concerns the gene NFKB1 and acute respiratory distress syndrome.