A previous report suggested that defects in T cell suppression observed in SLE patients are due to CD4+CD25− effector-cell resistance and not abnormal CD4+CD25+Foxp3+ Treg cell function [23], whereas a separate study demonstrated that Treg cells from BWF1 mice are not predisposed to functional incompetence, but rather are present in a highly activated state [24]. Here, FOXP3 is linked to systemic lupus erythematosus.