Increasing studies have reported that BET proteins were involved in the canonical NF-κB activation pathway in autoinflammation disorders, injury, infection, and chronic morbid conditions, and inhibition of the BET protein function effectively suppresses the NF-κB-mediated pro-inflammatory expression, alleviating the neuroinflammation response in these pathological conditions (Jahagirdar et al., 2017; Wang et al., 2018; Sánchez-Ventura et al., 2019; Zhou et al., 2019). The gene discussed is NFKB1; the disease is infection.