The longer survival of autoreactive T cells contributed to the persistence of a longer immune response.133 The low level of IL-2 in SLE was attributed to increased PP2AC expression and inhibition of AP1 activity in SLE T cells through suppression of the binding of phosphorylated cAMP-response element binding protein (CREB) to the cfos and IL-2 promoter.134. The gene discussed is JUN; the disease is systemic lupus erythematosus.