The fact that these peripheral murine tumours cannot develop in the presence of ova-induced stimulation of the transgenic TCR and have lost endogenous TCR expression is strikingly similar to the widely recognized absence of TCR expression and signalling9, 10, despite prior clonal TCR rearrangement, in human ALCL, and suggest that persistent co-existence of TCR and NPM–ALK-driven signalling in the periphery is not compatible with ALCL development and/or survival. This evidence concerns the gene ALK and anaplastic large cell lymphoma.