Tregs from patients with SLE had a defect in inhibition of IL-2R desensitization, pSTAT5 levels were initially lower in the Tregs from the patients, and STAT5 phosphorylation in response to low-dose IL-2 and was lost more rapidly in the Tregs from the disease patients compared to the Tregs from healthy controls (Figure 2). This evidence concerns the gene IL2 and systemic lupus erythematosus.