The pretreatment of bone marrow-derived macrophages (BMDMs) with the ferroptosis inducer erastin significantly attenuates the expression of proinflammatory cytokines (e.g., inducible nitric oxide synthase, tumor necrosis factor- (TNF-) α, and interleukin- (IL-) 1β) induced by lipopolysaccharide (LPS) treatment, and these effects are mediated by inhibition of the phosphorylation of IκB kinase β (IKKβ) and the phosphorylation and degradation of IκBα and NF-κB and thereby lead to the suppression of sepsis development [80]. This evidence concerns the gene NFKB1 and Sepsis.