NFKB1 and inflammatory bowel disease: In conclusion, our current study shows that EA, at a physiologically relevant dose, significantly improves systemic symptoms along the gut–liver–brain axis (Figure 1) in DSS-induced IBD mice by suppressing the expression of pro-inflammatory cytokines and inflammatory mediators through preventing the activation of NF-κB and MAPK pathways, oxidative/nitrative stress, gut dysbiosis, and intestinal barrier dysfunction.