Although our model recapitulates many aspects of human marginal-zone lymphoma biology, we think it has limitations that include the long tumour latency (which on the other hand reflects the slow development of SMZL observed in patients), and the fact that tumours are triggered by the activation of NKX2-3 in B cells, which is only observed in a fraction of patients with MALT lymphoma and SMZL. The gene discussed is NKX2-3; the disease is splenic marginal zone lymphoma.