Nur77 is a transcription factor that is induced to a high level during TCR‐mediated apoptosis of thymocytes and T cell hybridomas. Expression of a dominant‐negative mutant of Nur77 can inhibit TCR‐mediated apoptosis, while constitutive expression of full‐length Nur77 in thymocytes leads to massive apoptosis. Nur77 is similar to the steroid receptor family and consists of a transactivation, a DNA‐binding and a C‐terminal “ligand‐binding” domain. In contrast to the other nuclear receptors, Nur77 activity does not appear to depend on any ligand. However, its C‐terminal region can regulate its transactivation activity. A short C‐terminal deletion results in a protein with only 15 – 20 % activity while deletion of the entire C‐terminal region increases its activity. To further study the role of Nur77 transcription in apoptosis, we have generated transgenic mice expressing Nur77 with a short C‐terminal deletion or Nur77 without its entire C‐terminal domain. Mice expressing the shorter deletion / transcriptionally less active mutant displayed a mild phenotype. However, mice with the larger deletion / more transcriptionally active mutant showed massive thymocyte apoptosis. These data suggest that Nur77 transcription correlates with its apoptotic function in vivo.