Chronic Myeloid Leukemia (CML) has always been an ideal model to understand the 
molecular pathogenesis of human leukaemias and the way to cure them. This can be 
ascribed to the fact that CML was the first human cancer demonstrated to be 
strongly associated to the presence of a recurrent chromosomal translocation 
(the t(9;22)(q34;q11) that creates the Philadelphia (Ph)-chromosome) and to a 
specific molecular defect, the formation of a hybrid BCR-ABL gene that generates 
new fusion proteins endowed with a constitutive tyrosine-kinase (TK) activity, 
strongly implicated in the pathogenesis of the disease. The introduction into 
clinical practice of imatinib, (Glivec, Gleevec, Novartis), a potent tyrosine 
kinase inhibitor of the Bcr-Abl protein as well as of a restricted number of 
other TKs, has not only produced a substantial improvement in the treatment of 
CML, but represents a major break-through in the perspective of opening a new 
era, that of molecularly targeted therapy, in the management of other types of 
leukemia, lymphoma and cancer in general.