The reciprocal t(9;22)(q34;q11) translocation is identified as the initial transforming event in the pathogenesis of CML that yields a truncated chromosome 22 called the Philadelphia (Ph) chromosome [2] harboring the BCR-ABL fusion gene which constitutes the molecular basis of the disease [3]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.