Lymphocytes exist in a dynamic state that alternates between small quiescent cells and large, antigen-activated, proliferating cells. Their failure to activate properly or to turn off a proliferative program is a likely step in the development of lymphoid malignancies. Understanding the genetic mechanisms that regulate the expression of the alternately quiescent and activated phenotypes is a fundamental question for immunology and oncology. Significant progress in the identification of DNA elements that appear to play a role in the regulation of proliferation and differentiation has come about as a consequence of the isolation of oncogenes, pieces of genetic information that are involved in the malignant transformation of cells. Oncogenes were first isolated as part of the small genomes of rare RNA tumor viruses, called acute transforming retroviruses. These viruses effi ciently transform cells in culture and in animals. Acute retroviruses are