Macrophages are critically involved in the development and progression of ALI, as their polarisation toward a pro‐inflammatory phenotype contributes to the cytokine storm and subsequent tissue damage via activation of the TLR4/NF‐κB and MAPK signalling pathways, resulting in the excessive production of TNF‐α, IL‐6 and IL‐1β [32, 33]. The gene discussed is TLR4; the disease is acute respiratory distress syndrome.