Studies of mice deficient in the expression of the retinoid-related orphan receptor γ (ROR γ), a member of the nuclear receptor superfamily, have demonstrated that this receptor plays a crucial role in the regulation of thymopoiesis and lymph node organogenesis. Moreover, ROR γ-null mice are highly susceptible to early onset of thymic lymphoma. The number of both PCNA- and TUNEL-positive cells are increased in the thymus of ROR γ-null mice and thymic lymphomas compared to thymus of wild type mice. Dysregulation of proliferation and apoptosis in the thymus of ROR γ-null mice may disturb normal homeostasis and enhance the probability of individual cells to acquire mutations and, as a consequence, lead to a high incidence of T-cell lymphoma development. For details, see the article by Ueda et al. on page 901 of this issue.