By analyzing the serine312 phosphorylated form (p-Ser312) of IRS-1 and activation with phosphorylation of protein kinase (AKT) variations before and after anti-TNF therapy in RA patients, the mechanisms of its improvement in RA patients with IR might be due to p-Ser312IRS-1 levels decreasing and the proportion of activation with phosphorylation of AKT increasing after the anti-TNF therapy [45]. This evidence concerns the gene TNF and rheumatoid arthritis.