Studies of peripheral blood Tregs in patients with SLE have shown decreases in Treg numbers and defective Treg phenotypes.30 In patients with active lupus nephritis, urinary FOXP3 mRNA is increased compared with patients with inactive lupus and healthy controls.31 This could be explained by a transient activation of Foxp3 in activated effector T cells in humans32, 33 or may conceptually be consistent with a regulatory cell:effector cell ratio (rather than an absolute number) being more relevant in tissue injury. This evidence concerns the gene FOXP3 and lupus nephritis.