In this issue of Blood, Zlotoff and colleagues demonstrate the dysregulation that occurs after irradiation to the process of active importation of T-lineage progenitors into the thymus to seed T-cell development. In the steady state, thymic entry relies on the continuous importation of BM-derived progenitors from the circulation into available intrathymic niches, where instructive signals from the supporting microenvironment guide T-cell development. This process of importation is actively regulated by the interactions between PSGL-1/p-selectin, CCL25/CCR9, and CCL19-CCL21/CCR7. Zlotoff et al demonstrate disrupted processes that occur after irradiation that ultimately lead to impaired thymic reconstitution. These are: (1) reduced supply of capable thymic seeding progenitors from the BM, (2) uncoupling of the dependence of thymic importation on CCR9/CCL25 and CCL19-CCL21/CCR7, and (3) extended periods in the thymus where niches remain unsaturated. All of this leads to reduced development of T cells and output into the periphery. These findings provide a potential target for enhancing engraftment of precursor T cells and thymic reconstitution.