Pathogens activate the innate immune response of epithelial cells and alveolar macrophages, followed by migration and aggregation of neutrophils and monocytes, release of the inflammatory cytokines TNF-α, IL-1β, and IL-6, loss of alveolar-capillary barrier integrity, and increased permeability, leading to sepsis-associated ALI/ARDS (Luyt et al., 2020). The gene discussed is IL1B; the disease is acute respiratory distress syndrome.