Angioimmunoblastic lymphadenopathy (AIL) still is a clinico-pathological syndrome with little known physiopathology. The advent of molecular biology has improved our understanding of this syndrome by characterization of the clonal cell. With this technique, combined with cytogenetics and immunohistochemistry, three pathological states have been individualized: 1) true AIL without evidence of monoclonal proliferation; 2) transformed AIL, and 3) AIL-like T-cell lymphoma. This clinical complex can be integrated in an evolutive continuum, starting with simple lymphoid hyperplasia and ending with frank malignant T-cell lymphoma.