Rheumatoid Arthritis studies revealed that phosphorylation of FOXO3a took place in lymphocytes and when FOXO3a deficient mice were stimulated for proliferation, spontaneous lymphoproliferation was observed along with inflammation of organs such as salivary glands, lungs, and increased activity of helper T cells, supporting an important role for FOXO3a in preventing T cell hyperactivity which is one of the premier causes of asthmatic inflammation [20]. This evidence concerns the gene FOXO3 and rheumatoid arthritis.