IL1B and Insulin resistance: IκB retains NF-κB in an inhibitory cytoplasmic complex at a steady-state, and IKK phosphorylation could phosphorylate IκBα under inflammation, which separates and degrades IκBα from NF-κB [151], allowing free NF-κB to translocate to the nucleus and interact with related DNA response elements binding, which induces transactivation of inflammatory genes such as TNF-α, IL-1β, and IL-6, further contributing to insulin resistance [152].