The discovery that a regulatory subset of CD4+ T cells (Treg) modulates the activity of effector Th1 and Th2 responses in mouse models of schistosomiasis [14] has led to suggestions that it is the balance between effector and regulatory responses including Treg, which determines the outcome of murine helminth infections [15], has also been postulated for human helminth infections [16], [17]. The gene discussed is CD4; the disease is helminthiasis.