The ability of ES-62 to suppress pathogenic B cell and effector cell responses appears to be associated with a homeostatic resetting of the effector cell–to–regulatory cell balance, as indicated by the reduction in the frequency of pathogenic plasmablasts and the increased number of CD19+CD23+CD21+ B cells with the capacity to produce IL-10, a phenotype reminiscent of the regulatory B cells proposed to be defective in MRL/lpr mice 28 and SLE 27. The gene discussed is CD19; the disease is systemic lupus erythematosus.