In another study with PAD4 (PAD4−/−) deficient mice, the mice were partially protected from lipopolysaccharide‐induced shock, suggesting that PAD4/NETs may contribute to the toxic inflammatory and procoagulant host response to endotoxin.7 Recently, Biron et al8 also showed that Cl‐amidine treatment, an inhibitor of PAD4, prior to cecal ligation and puncture, improved overall survival in sepsis. The gene discussed is PADI4; the disease is Sepsis.