**1. Introduction**

Leukemias are clonal and acquired diseases of the hematopoietic stem cell or a precursor already committed to lymphoid and /or myeloid lineages [1]. hyperplasia produced a tissue that results from cell proliferation as myeloid pathology. Chronic myeloid leukemia (CML) is a monoclonal pathology of the pluripotent stem cell characterized by neoplastic granulocytic overproduction. This myeloproliferative syndrome has two particular characteristics:


is generated from the reciprocal translocation involving the q34 band of chromosome 9 and the q11 band of chromosome 22.

The recent development of therapeutics targeted at the activity or stability of an oncogenic protein has recently been illustrated by the therapeutic successes obtained in the treatment of chronic myeloid leukemia and acute promyelocytic leukemia [1]. Until now cytogenetics has been the reference for structural abnormalities, in particular translocations, tools for precise diagnosis in certain disputed cases and the detection of residual diseases or possible relapses. However molecular cytogenetics can detect chromosomal abnormalities of small sizes not visible on metaphasic chromosomes (semi-cryptic). It is of particular interest in the analysis of acquired abnormalities and is involved in monitoring the persistence of an abnormal clone in order to detect predicted recurrent translocations and may also help characterize genes in the evolutionary process of carcinogenesis. The current recommendations are based on highquality evidence reported in peer-reviewed journals, supplemented by expert group consensus. These recommendations apply to healthcare professionals who treat CML patients and CML patients to better understand their conditions and treatments [2].
