Similarly, genetic ablation of Stat1 on the background of a mouse that has enhanced TLR4 signaling (because of deletion of Il6st, a key regulator of systemic inflammatory responses during LPS-mediated endotoxemia) provides protection against LPS-induced toxemic death compared to mice with normal STAT1 levels (Luu et al., 2014). Here, STAT1 is linked to serum lipopolysaccharide activity.