TLR4-mediated and CD40-mediated signals received by macrophages during early endotoxemia are known to promote IL-10 transcription, which can in turn signal to degrade mRNA encoding TNFα (Inoue et al., 2014), thus identifying IL-10 as a crucial feedback control molecule that mediates cessation of inflammation. The gene discussed is TNF; the disease is serum lipopolysaccharide activity.