Tolerance is a developmentally acquired property of the vertebrate immune system, in part ensured by regulatory CD4⁺ lymphocytes (Treg cells) expressing the Foxp3 transcription factor. Recent work has shown that thymic emigrants are the preferential source of peripherally generated Treg cells. A new report in this issue of the European Journal of Immunology [Eur. J. Immunol. 2013. 43: 2598–2604] describes a cell autonomous defect in Foxp3 induction in aged CD4⁺ cells in mice. Immune homeostasis becomes progressively less robust as ontogeny gives way to aging, and a key feature of senescence is thymic involution and the impaired T‐cell turnover that follows. In this Commentary, we discuss the implications of these recent findings for our understanding of the induction of tolerance to peripheral antigens in aging.