It remains poorly understood whether the metabolic effects are mediated by IKK or NF-κB activity, but because the NF-κB-mediated gene transactivation in our model is not further increased upon hepatocytic A20-deficiency and A20 ablation alone does not result in steatosis, we speculate an essential role for the IKK complex in controlling DNL and cholesterol synthesis [40]. The gene discussed is TNFAIP3; the disease is steatosis.