Foxo transcription factors have a conserved role in the adaptation of cells and organisms to nutrient and growth factor availability. Here we show that Foxo1 has a crucial, nonredundant role in T cells. In naive T cells, Foxo1 controlled the expression of the adhesion molecule L-selectin, the chemokine receptor CCR7 and the transcription factor Klf2, and its deletion was sufficient to alter lymphocyte trafficking. Furthermore, Foxo1 deficiency resulted in a severe defect in interleukin 7 receptor α-chain (IL-7Rα) expression associated with its ability to bind an Il7r enhancer. Finally, growth factor withdrawal induced a Foxo1-dependent increase in Sell, Klf2 and Il7r expression. These data suggest that Foxo1 regulates the homeostasis and life span of naive T cells by sensing growth factor availability and regulating homing and survival signals.Throughout adult life, the number and diversity of peripheral T cells depends on de novo cell development and cell division, balanced against programmed cell death. A growing number of studies show that this 'homeostasis' of T cells is controlled by cytokines, such as interleukin 7 (IL-7), as well as by interactions between T cell antigen receptor (TCR) and major histocompatibility complex (MHC) 1, 2. However, the cell-intrinsic factors responsible for the integration of environmental signals and the manner in which they manifest changes in cell populations remain poorly defined.The Foxo subfamily of transcription factors has a highly conserved role in the regulation of life span, cell cycle progression, apoptosis, glucose metabolism and stress resistance by integrating information pertaining to the abundance of nutrients, growth factors and stress signals 3 . In mammals, the Foxo subfamily consists of four members: Foxo1 (A000944),