T cell homeostasis and function have to be tightly regulated to combat infectious diseases, cancer and to avoid autoimmunity. On a molecular level several factors are needed to regulate the expression of involved genes. Nuclear receptor corepressor 1 (NCOR1) is one of them. NCOR1 is a transcriptional regulator that bridges repressive chromatin modifying enzymes such as histone deacetylases (HDACs) with transcription factors and is implicated in many biological processes, however its role in T cells is not known. Originally NCOR1 was identified as a corepressor of nuclear receptor-mediated gene repression but it was also shown that NCOR1 interacts with members of the BTB zinc finger (BTB-ZF) transcription factor family such as PLZF, BCL6 and MAZR, which are key regulators of T cell development and function. Here we show that Cd4Cre-mediated deletion of NCOR1 (NCOR1 cKO^Cd4) resulted in a reduction of peripheral T cell numbers due to a decrease in single-positive (SP) thymocytes. In contrast, double-positive (DP) thymocyte numbers were not affected in the absence of NCOR1. The reduction in SP cells was due to diminished survival of signaled NCOR1-null CD69⁺ thymocytes. NCOR1-null thymocytes expressed elevated levels of the pro-apoptotic factor BIM and, upon ex vivo TCR/CD28 stimulation, showed a higher fraction of cleaved Caspase 3-positive cells. However, staphylococcal enterotoxin B (SEB)-mediated negative selection of Vβ8⁺ CD4SP thymocytes was not changed, suggesting that this process is not altered in the absence of NCOR1. Finally, transgenic expression of the pro-survival protein BCL-2 restored the fraction of CD69⁺ thymocytes in NCOR1 cKO^Cd4 mice to a similar percentage as observed in wild-type mice. Together, these data identify NCOR1 as a crucial regulator of the survival of signaled CD69⁺ thymocytes during the DP to SP transition and revealed that NCOR1 is essential for the proper generation of the peripheral T cell pool.