Indeed, it was shown in murine and later also in human SLE that an acquired and progressive deficiency of the cytokine interleukin-2 (IL-2), an essential growth and survival factor for Treg, promotes an imbalance between Treg and effector/memory CD4+ T cells, which was associated with accelerated disease activity (16–18). This evidence concerns the gene IL2 and systemic lupus erythematosus.