Upregulation of Octn1 and activation of stellate cells, after treatment with the liver toxin dimethylnitrosamine, were seen to lead to increased liver levels of the natural, nutrient-derived, OCTN1 substrate, antioxidant ergothioneine, which resulted in protection from inflammation, oxidative stress, and more severe liver fibrosis [90]. This evidence concerns the gene SLC22A4 and Hepatic fibrosis.