CML is characterized by the t(9;22)(q34;q11) reciprocal translocation and the consequent generation of a chimeric BCR/abl oncogene, encoding for a 210-kDa fusion oncoprotein (BCR/Abl), endowed with constitutive tyrosine kinase activity, which is essential for CML onset, maintenance and progression [1]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.