The activated TAK1 further lead to an activation of downstream MKK–JNK–IRS1307 and IKKβ–NF-κB signalling, and an inhibition of AKT–GSK3β/FOXO1 phosphorylation cascades, facilitating the insulin resistance, inflammatory response and glucose metabolic disorder in the liver, thereby exacerbating fatty acid accumulation and the resultant hepatic steatosis (Fig. 10). This evidence concerns the gene GSK3B and glucose metabolism disease.