Given that CCR4 plays a crucial role in attenuating immunoinflammatory responses in autoimmune or allergic disease via the modulation of Treg function (Yuan et al., 2007; Faustino et al., 2013), we speculated that despite the expansion and unaltered expression of activation- or function-associated molecules in Tregs, these cells might be dysfunctional. The gene discussed is CCR4; the disease is allergic disease.