As TNF-α can modulate endotoxin-induced upregulation of IL-1β and IL-6 [8,13,16], we thus conjectured that the SEM18 peptide can decrease the endotoxemia-induced upregulation of IL-1β and IL-6 in plasma and lung tissues as well as the endotoxemia-induced bindings of IL-1β/IL-1R and IL-6/IL-6R in lung tissues. The gene discussed is IL1R1; the disease is serum lipopolysaccharide activity.