Immunogenetic analysis of human ALCL demonstrated that the majority have major in-frame, potentially selected, TCRα receptor rearrangements in the absence of comparable TCRβ rearrangements, in keeping with the absence of detectable TCRβ protein, compatible with replacement of TCRβ by NPM–ALK in the development of classical ALCL. The gene discussed is ALK; the disease is anaplastic large cell lymphoma.