These include but are not limited to lipopolysaccharide hypersensitivity of alveolar macrophages [50,51]; enhanced signal transduction via NF-κB and MAPK pathways [50,52]; altered LPS-induced metabolic pathways [52]; impaired apoptosis of neutrophil granulocytes [53,54]; and an increased release of various proinflammatory cytokines [50,55], including IL-17 [56,57] and IL-6 [58,59], known as key contributors in the development of AIDs [60]. The gene discussed is NFKB1; the disease is AIDS.