FOXN1 and thymus atrophy: To determine whether the capacity of newly generated tTreg cells is impaired in aged thymus [17] and/or in the TEC defect-induced atrophied thymus, we utilized our previously generated mouse model with accelerated thymic atrophy (due to postnatal TEC homeostatic defect) [12], in which the loxp-flanked FoxN1 gene (FoxN1fx/fx) [18] can be deleted by ubiquitous promoter-driven Cre-recombinase and estrogen-receptor fusion protein (CreERT) mediation through either a tamoxifen (TM) induction or a CreERT autoleakage with age.