“…The demonstration that rearrangement of genomic fragments of the CMYC oncogene coincide with Ig gene rearrangement clinched this proposal (Dalla-Favera et al, 1982;Taub et al, 1982) and subsequent cloning of translocated CMYC revealed many features of the mechanism and consequences of chromosomal translocations (reviewed in . The association of the rearranging antigen receptor genes with chromosomal translocations in leukaemia was taken further when the T cell receptor (TCR) b chain locus was mapped to chromosome 7, band q35 (Rabbitts et al, 1985), suggesting that chromosomal translocations in T cell tumours are mediated by the intrinsic chromosomal instability of TCR genes, which undergo rearrangement in normal lymphoid lineage development. This was con®rmed by cloning of LMO1 and LMO2 at chromosomal translocation junctions with TCRd and TCRa (Boehm et al, 1988aMcGuire et al, 1989;Royer-Pokora et al, 1991) and of HOX11 and LMO2 at chromosomal translocations with TCRb Dube et al, 1991;Hatano et al, 1991;Kennedy et al, 1991;Lu et al, 1991).…”