The localization of cellular oncogenes near the break points of tumour-specific chromosomal aberrations suggests an involvement of these genes in the generation of neoplasms^1,2. Recently, we demonstrated³ the translocation of the human cellular homologue (c-abl) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) from chromosome 9 to the Philadelphia chromosome (Ph¹) in chronic myelocytic leukaemia (CML). In an attempt to investigate the significance of this translocation in the pathogenesis of CML, we have now studied two CML patients with complex translations, t(9; 11; 22) and t(1; 9; 22), and two CML Ph¹-negative patients with apparently normal karyotypes. In addition to using blot hybridization with human c-abl probes and DNA from Rodent: CML cell hybrids as before, we have used in situ hybridization of these probes directly to metaphase chromosomes of CML patients. These studies show that the c-abl gene is translocated in Ph¹-positive but not in Ph¹-negative CML patients. CML without the Ph¹ chromosome seems to be a distince entity with a different origin, and this view is supported by clinical observations including correlations which reveal a poorer prognosis^4,5.