Therefore, in future studies, it is very important to identify the key factor(s) that interacts with IKK2-NF-kB during pathological conditions and switches the function of IKK2-NF-kB from liver protection to pro-inflammation and pro-fibrosis, which might allow us to selectively modulate the IKK-NF-kB pathways to improve the efficacy and decrease the toxicity of drug treatment of metabolic syndrome, infectious/inflammatory diseases, and liver diseases. Here, NFKB1 is linked to metabolic syndrome.