TRIM16 recognizes phosphorylated TAK1 through its B-box structural domains and catalyze K48-linked protein ubiquitination modifications, leading to the degradation of phosphorylated TAK1, which in turn attenuates its phosphorylation of downstream JNK/p38, ameliorates IR, and reduces the expression of genes related to fatty acid metabolism in the liver, and attenuates lipid accumulation and inflammatory response during the progression of NASH (28). This evidence concerns the gene MAPK8 and metabolic dysfunction-associated steatohepatitis.