In addition, the expansion of the FOXP3+ Tregs in SLE patients was higher in the memory CD45RA− compartment (Figures 1D,E) compared to the naïve CD45RA+ compartment (Figures 1D,F), suggesting that the observed increased Treg frequency is not a direct effect of an increased thymic Treg output in SLE patients, but rather is a regulatory response to the inflammation caused by activated immune cells mediating the autoimmune disease. The gene discussed is FOXP3; the disease is autoimmune disease.