Although the latter explanation of a negative regulation of Foxp3+ Treg cells by IL-4Rα signaling in favor of ex-Foxp3 transdifferentiation can be appropriately dismissed by using fate-reporter mice, our present study, as it stands, convincingly indicates that the T cells responsible for the increased cytokine production reported in Foxp3cre IL-4Rα−/lox diseased mice expressed not Foxp3 but rather GATA3, a profile inconsistent with recently reported ex-Foxp3 T cells during helminth infections [18]. The gene discussed is FOXP3; the disease is helminthiasis.