The byproducts of methionine metabolism in ALD (marked by the lowered SAMe levels leading to competitive inhibition of most methyltransferases and upregulated demethylated product as homocysteine [44] and its derivatives such as SAH [8]) interact with proinflammatory cytokines (such as TNF-α), subsequently potentiating hepatotoxicity and fatty liver [17]. This evidence concerns the gene TNF and Hepatic steatosis.