The relative contribution of defects in B cell anergy to SLE pathogenesis has been of particular interest, as lupus patients show increased activation of cells with an anergic phenotype in the mature B cell compartment [2,3]; however, it is unknown whether these cells directly differentiate into antibody-secreting cells (ASCs) or instead act to inhibit endogenous antibody production by inhibiting CD4+ T cell activation [4] and/or inducing regulatory T (Treg) cells [5–7], as has been shown for some anergic B cell populations. Here, CD4 is linked to systemic lupus erythematosus.