Several previous studies determined that, following infection, RV could interact with IRF3 and NF-κB, and result in the proteasome-mediated degradation of IRF3 and NF-κB, and then suppress host’s normal immune antiviral immune response and cytokines secretion, which is one of the reasons that RV lead to a severe gastroenteritis (63, 64). This evidence concerns the gene NFKB1 and gastroenteritis.