TNF-α activity on insulin resistance can be explained as follows: it increases the release of free fatty acids (FFA) in adipocytes; it blocks the synthesis of adiponectin, which possesses insulin-sensitizing activity in high concentrations in adipose tissue, and it interferes with the activity of tyrosine-residue phosphorylation activity in the first substrate of the insulin receptor, which is necessary for progression of the intracellular signal of the hormone [3]. This evidence concerns the gene INSR and Insulin resistance.