Chronic myeloid leukemia (CML) represents an important paradigm for understanding the molecular events leading to malignant transformation of primitive hematopoietic progenitors. LSCs are rare and divide less frequently, and thus, represent a reservoir for relapse and resistance to a molecularly targeted single agent the. LSCs are able to evade the majority of current cancer treatments that target rapidly dividing cells. The success of tyrosine kinase inhibitors at controlling the chronic phase disease is tempered somewhat by the persistence of the LSC pool in the majority of the patients. Combined therapies targeting aberrant properties of LSC may obviate therapeutic resistance and relapse in advanced phase and therapeutically recalcitrant CML. CD7 antigen is expressed on immature myeloid progenitor of chronic phase-chronic myeloid leukaemia patients with inferior survival as a consequence of the more immature CD34+CD7+ stem cell carrying t (9;22). Our work is to preliminary understand the origin of malignant stem cells in CML as well as to study the incidence of very primitive CML stem cells among different CML cases so as to anticipate the ontogeny as well as the prognosis. In-addition, this study aims to pave the way for further studies on CML initiating stem cells.