In the current context, an increased circulating sIL-7R concentration can potentiate IL-7 bioactivity and promote autoimmunity in vivo, through a mechanism by which the sIL-7R is able to compete with cell-associated IL-7 receptor and diminish excessive IL-7 consumption, sequentially enhances proliferative responses of T-cells to weak self-antigens, and leads to autoimmune diseases, such as type I diabetes, RA, MS, and SLE [24, 25, 30]. This evidence concerns the gene IL7R and rheumatoid arthritis.