A single genetic lesion, the t (9,22) reciprocal translocation which generates the BCR-ABL1 rearranged gene, is the causative event of CML, driving clonal expansion of leukemic hematopoiesis via the constitutive activation of BCR-ABL1 TK [1]. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.