Since the identification of human Notch1 as a gene involved with a t(7;9)(q34;q34.3) chromosomal translocation in a subset of patients with T-ALL [1], several studies have implicated dysregulated Notch signalling in the aetiology and pathogenesis of T-ALL: Mice transplanted with bone marrow cells transduced with a constitutively active form of Notch1 develop T cell neoplasms [2], while mice transgenic for constitutively active form of Notch3 [3] develop thymic lymphomas. Here, NOTCH1 is linked to thymus lymphoma.