Moreover, the aforementioned enhancement of survival and Foxp3 expression of CD4+ CD25+ Treg cells upon induction of IL-4/IL-4Rα-mediated signaling in vitro and the striking higher expression of IL-4Rα by Foxp3+ Treg cells observed during infection warranted us to further address the possible higher need for this receptor by Foxp3+ Treg cells, in vivo, during inflammatory disease conditions. The gene discussed is IL4R; the disease is infection.