As a special tumor, chronic myeloid leukemia (CML) is a clonal myeloproliferative disease, characterized by the oncogenic Philadelphia chromosome, formed by a reciprocal translocation between chromosomes 9 and 22, resulting in the novel chimeric protein BCR/ABL (breakpoint cluster region, BCR; Abelson murine leukemia viral oncogene, ABL), that dictates the pathophysiology of CML [10]–[12]. The gene discussed is BCR; the disease is neoplasm.