The ASK1‐JNK‐p38 pathway was found to be overactivated in several animal models of NASH,12, 13 and blocking ASK1 N‐terminal dimerization and autophosphorylation with a short CFLAR peptide or administering the ASK1 inhibitor GS‐444217 significantly ameliorated NASH symptoms.14, 15. This evidence concerns the gene MAPK8 and metabolic dysfunction-associated steatohepatitis.