As Tfh cells contribute to survival, affinity maturation, isotype class-switching, and differentiation of germinal center B cells (9), it is likely that exacerbated SLE-like symptoms in S4B6/IL-2-pretreated mice resulted from enhanced germinal center reactions leading to augmented production of pathogenic autoantibodies. The gene discussed is IL2; the disease is systemic lupus erythematosus.