We demonstrated previously that blocking Gβγ signaling resulted in potentiation of TCR-stimulated IL-2 mRNA increases in human CD4+ T helper cells [1], suggesting this approach might be useful for treating autoimmune diseases, as low dose IL-2 therapy effectively suppressed immune responses in chronic graft-versus-host disease [2] and hepatitis C virus-induced vasculitis [3]. The gene discussed is IL2; the disease is vasculitis.