NOX4 was not only upregulated in myofibroblastic foci in IPF, but also in nonalcoholic steatohepatitis and in hepatitis C virus-induced fibrosis [[10], [11], [12]], and deleting the Nox4 gene proved beneficial in several animal models of lung and liver fibrosis [[13], [14], [15], [16]]. This evidence concerns the gene NOX4 and metabolic dysfunction-associated steatohepatitis.