Breakpoints on chromosome 11 at band q23 have been observed in patients with primary or secondary leukaemia. Recent data have shown that these breakpoints are clustered in a approximately 15kb region of a gene named HRX. This gene product has homology to the Drosophila trithorax gene product, which suggests it may play a role in regulating transcription control. Disruption of HRX as a result of chromosomal translocation is thought to contribute to the leukaemogenic process; this may occur in utero giving rise to infant acute leukaemia or may be induced by epipodophyllotoxic drugs resulting in secondary leukaemia. Translocations of 11q23 can involve a number of different partner chromosomes. The reciprocal genes on chromosomes 4q21, 9p22 and 19p13 have been recently cloned and are predicted to encode proline and serine rich proteins. Of particular interest is the high degree of homology observed between the genes on 9p22 and 19p13, which suggests that they too may have an important role to play in the generation of the leukaemic phenotype.