Increased oxidative and nitrosative/nitrative stress, through elevated and/or activated liver CYP2E1, NADPH oxidase, and iNOS, can play an important role in promoting ALD and the activation of hepatic stellate cells for liver fibrosis, since genetic deletion or using specific inhibitors of these pro-oxidant enzymes significantly attenuated the levels of ALD in various rodent and cell culture models [24,35,36,37,38,39,40]. The gene discussed is NOS2; the disease is Hepatic fibrosis.