In support of the former, NPM1-ALK enables thymocytes to skip beta-selection in mice, and it has been observed that two-thirds of human ALCL tumours have TCR rearrangements that would not normally be permissive of successful thymic development suggesting that NPM1-ALK is active in the aberrant thymocytes of children carrying this translocation [7,20]. This evidence concerns the gene ALK and neoplasm.