In the lipopolysaccharide (LPS)/sepsis-induced ALI model, activation of JAK-STAT3 signaling in lung epithelial cells and alveolar macrophages upregulated pro-inflammatory cytokines [IL-6, IL-1β, tumor necrosis factor-alpha (TNF-α)] and chemokines (CC chemokine receptor 2, C-X-C motif chemokine ligand 15) (46–52). This evidence concerns the gene TNF and Sepsis.