Interestingly and in sharp contrast to the phenotype observed in Casp8ΔIEC mice, additional deletion of Stat1 in these mice (Casp8ΔIECxStat1−/− mice) could protect from severe endotoxemia, body weight loss and lethality (Fig. 1A, C). The gene discussed is STAT1; the disease is serum lipopolysaccharide activity.