The non alcoholic steatohepatitis is a more and more frequent disease. Great progress in the physiopathologic mechanisms has been recently observed. The mitochondrial dysfunction seems to be the main mechanism implied in the necroticoinflammatory genesis of the non alcoholic steatohepatitis lesions. When this one is of metabolic origin, this dysfunction occurs on a vulnerable to aggressions steatosis liver. Several implied factors leads to the increased liberation of free radicals that will activate the lipidic peroxydation. This one is considered as the main generator of necroticoinflammatory lesions and fibrosis. The future therapeutic alternatives depends on a better comprehension of mitochondrial dysfunction.