Recent reports suggested that several other DUSPs such as DUSP9, DUSP12, and DUSP26 had the protective effects on the development of nonalcoholic steatohepatitis in mice, and the expressions of those DUSPs decreased in the disease condition [16,17,18], supporting the concept that the overexpressed DUSP5 may play a role in the process of diverse liver diseases at different stages. This evidence concerns the gene DUSP26 and metabolic dysfunction-associated steatohepatitis.