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). The gene discussed is IL2RA; the disease is systemic lupus erythematosus.