The study of cellular oncogenes and of chromosomal abnormalities in human tumours has, in several instances, suggested a link between a specific oncogene translocation and oncogenesis. It was recently suggested that the translocation of the c-abl gene (the human cellular homologue of the transforming sequence of Abelson murine leukaemia virus) from chromosome 9 to 22 in Philadelphia translocation, might have a role in the generation of chronic myeloid leukaemia (CML). We propose an alternative hypothesis and suggest that the translocation of another gene, c-sis, may be more important.