The transforming genes of oncogenic retroviruses are homologous to a group of evolutionary conserved cellular onc genes¹. The human cellular homologue (c-abl) of the transforming sequence of Abelson murine leukaemia virus (A-MuLV) was recently shown² to be located on chromosome 9. The long arm of this chromosome is involved in a specific translocation with chromosome 22, the Philadelphia translocation (Ph¹), t(9;22) (q34, q11), which occurs in patients with chronic myelocytic leukaemia (CML)^3–5. Here we investigate whether the c-abl gene is included in this translocation. Using c-abl and v-abl hybridization probes on blots of somatic cell hybrids, positive hybridization is found when the 22q⁻(the Philadelphia chromosome), and not the 9q⁺ derivative of the translocation, is present in the cell hybrids. From this we conclude that in CML, c-abl sequences are translocated from chromosome 9 to chromosome 22q⁻. This finding is a direct demonstration of a reciprocal exchange between the two chromosomes⁶ and suggests a role for the c-abl gene in the generation of CML.