Remarkably, it has been shown that in patients with systemic lupus erythematosus (SLE), the CD19+CD24hiCD38hi B subset produces less IL-10 in response to CD40 stimulation and is unable to inhibit Th responses, suggesting that altered cellular function of the subpopulation in SLE may impact the immune effector responses in this autoimmune disease [4]. Here, CD19 is linked to autoimmune disease.