ATF3 has been shown to cross-talk to NF-κB and to act as a negative regulator of pro-inflammatory responses in different settings, such as preeclampsia (Kaitu’U-Lino et al., 2017), inflammation after cerebral injury (Wang et al., 2012), and Toll-like receptor 4 signaling (Gilchrist et al., 2006), in the latter case by direct binding to the p65/RelA subunit of NF-κB (Kwon et al., 2015). The gene discussed is TLR4; the disease is preeclampsia.