NFKB1 and Sepsis: Furthermore, tissue damage control and LPS-induced disease tolerance during sepsis was induced independent of interferon-α/β receptor (IFNAR) signaling (Figure 2J and Figure 2—figure supplement 1I) and the anti-inflammatory NF-κB subunit p50 (NF-κB1) (Figure 2K and Figure 2—figure supplement 1J), which has been shown to mediate the suppression of cytokine production during endotoxin tolerance in vitro (Fan and Cook, 2004; Ziegler-Heitbrock, 2001).