Interestingly, we found that GBP2 deficiency fails to significantly inhibit caspase-11-dependent immune responses in endotoxemia; whereas genetic deletion of GBP1, GBP2, GBP3, GBP5 and GBP7 simultaneously blocked endotoxemia-induced caspase-11 activation. The gene discussed is GBP2; the disease is serum lipopolysaccharide activity.