As low dose IL-2 therapy has shown promise for treating autoimmune diseases, effectively suppressing immune responses in chronic graft-versus-host disease [2] and hepatitis C virus-induced vasculitis [3], and part of the mechanism by which IL-2 counteracts autoimmunity may involve shifting CD4+ T helper cells from the TH1 and TH17 subtypes to the TH2 subtype [10, 11, 12, 13, 31, 32], we sought to determine whether blocking Gβγ signaling affected the balance between these T helper cell subtypes. The gene discussed is CFB; the disease is vasculitis.