Transcription factor NF-κB, whose activation depends on the IKKβ catalytic subunit of the IκB kinase, was assigned with both anti- and proapoptotic functions in T lymphocytes. To critically evaluate these functions, we transferred Ikkβ^−/− or wild-type (wt) fetal liver (FL) stem cells into lethally irradiated mice. Ikkβ^−/− radiation chimeras show thymic rudiments, aberrant lymphoid organs, and absence of T cells. T lymphopoiesis is rescued when Ikkβ^−/− stem cells are cotransferred with wt bone marrow, suggesting that IKKβ may mediate its lymphopoietic function via extrinsic factors. However, almost normal development of Ikkβ^−/− T cells is observed upon removal of type 1 TNFα receptor, indicating that TNFα signaling accounts for the absence of Ikkβ^−/− T cells. Indeed, Ikkβ^−/− radiation chimeras exibit elevated circulating TNFα, and Ikkβ^−/− thymocytes display increased TNFα sensitivity.